All of the genes located on a given chromosome comprise a a karyotype b bridging cross c wild-type allele d linkage group e none of these?

Allele that is the most common form of a gene in natural population or in a standard?

Wildtype!

Is it true or false a control group must be present in an experiment?

True!- Without a control group you have nothing to compare your experimental data with... so you cannot prove anything. An example: If you wish to test if a mutant plant grows better than a wildtype plant. You couldn't just grow the mutant plant and say it's better or worse than the wildtype if you haven't grown the wildtype plant aswell.

What does cell autonomous mean?

A genetic trait in multicellular organisms in which only genotypically mutant cells exhibit the mutant phenotype. eg. a transcription factor is usually cell autonomous. Conversely, a cell non-autonomous trait is one in which genotypically mutant cells can be rescued to wildtype phenotype by neighbouring genotypically wildtype cells. eg. A signalling factor will often have non-autonomous effects. There is also the very rare case of domineering non-autonomy in which genotypically mutant cells cause other cells (regardless of their genotype) to exhibit a mutant phenotype. eg. in types of polarity, where a mutant cell sends an incorrect polarity signal to the neighboring wildtype cell.

What are some disadvantages for genetically engineered animals?

Disadvantages of transgenic animals for humans include transgenesis not being good for the animals, altering of an animal's cells is not ethical, and the scientists that create transgenic animals have no way of knowing what the outcome will be. Adverse reactions are common and usually unexpected.

What is the results of a mutation?

Mutations are changes in the DNA sequence of a cell's genome and are caused by radiation, viruses, transposons and mutagenic chemicals, as well as errors that occur during meiosis or DNA replication.[1][2][3] They can also be induced by the organism itself, by cellular processes such as hypermutation.Mutation can result in several different types of change in DNA sequences; these can either have no effect, alter the product of a gene, or prevent the gene from functioning. Studies in the fly Drosophila melanogaster suggest that if a mutation changes a protein produced by a gene, this will probably be harmful, with about 70 percent of these mutations having damaging effects, and the remainder being either neutral or weakly beneficial.[4] Due to the damaging effects that mutations can have on cells, organisms have evolved mechanisms such as DNA repair to remove mutations.[1] Therefore, the optimal mutation rate for a species is a trade-off between costs of a high mutation rate, such as deleterious mutations, and the metabolic costs of maintaining systems to reduce the mutation rate, such as DNA repair enzymes.[5] Viruses that use RNA as their genetic material have rapid mutation rates,[6] which can be an advantage since these viruses will evolve constantly and rapidly, and thus evade the defensive responses of e.g. the human immune system.[7]Mutations can involve large sections of DNA becoming duplicated, usually through genetic recombination.[8] These duplications are a major source of raw material for evolving new genes, with tens to hundreds of genes duplicated in animal genomes every million years.[9] Most genes belong to larger families of genes of shared ancestry.[10] Novel genes are produced by several methods, commonly through the duplication and mutation of an ancestral gene, or by recombining parts of different genes to form new combinations with new functions.[11][12] Here, domains act as modules, each with a particular and independent function, that can be mixed together to produce genes encoding new proteins with novel properties.[13] For example, the human eye uses four genes to make structures that sense light: three for color vision and one for night vision; all four arose from a single ancestral gene.[14] Another advantage of duplicating a gene (or even an entire genome) is that this increases redundancy; this allows one gene in the pair to acquire a new function while the other copy performs the original function.[15][16] Other types of mutation occasionally create new genes from previously noncoding DNA.[17][18]Changes in chromosome number may involve even larger mutations, where segments of the DNA within chromosomes break and then rearrange. For example, two chromosomes in the Homo genus fused to produce human chromosome 2; this fusion did not occur in the lineage of the other apes, and they retain these separate chromosomes.[19] In evolution, the most important role of such chromosomal rearrangements may be to accelerate the divergence of a population into new species by making populations less likely to interbreed, and thereby preserving genetic differences between these populations.[20]Sequences of DNA that can move about the genome, such as transposons, make up a major fraction of the genetic material of plants and animals, and may have been important in the evolution of genomes.[21] For example, more than a million copies of the Alu sequence are present in the human genome, and these sequences have now been recruited to perform functions such as regulating gene expression.[22] Another effect of these mobile DNA sequences is that when they move within a genome, they can mutate or delete existing genes and thereby produce genetic diversity.[2]In multicellular organisms with dedicated reproductive cells, mutations can be subdivided into germ line mutations, which can be passed on to descendants through their reproductive cells, and somatic mutations, which involve cells outside the dedicated reproductive group and which are not usually transmitted to descendants. If the organism can reproduce asexually through mechanisms such as cuttings or budding the distinction can become blurred.For example, plants can sometimes transmit somatic mutations to their descendants asexually or sexually where flower buds develop in somatically mutated parts of plants. A new mutation that was not inherited from either parent is called a de novo mutation. The source of the mutation is unrelated to the consequence[clarification needed], although the consequences are related to which cells were mutated.Nonlethal mutations accumulate within the gene pool and increase the amount of genetic variation[23]. The abundance of some genetic changes within the gene pool can be reduced by natural selection, while other "more favorable" mutations may accumulate and result in adaptive evolutionary changes.For example, a butterfly may produce offspring with new mutations. The majority of these mutations will have no effect; but one might change the color of one of the butterfly's offspring, making it harder (or easier) for predators to see. If this color change is advantageous, the chance of this butterfly surviving and producing its own offspring are a little better, and over time the number of butterflies with this mutation may form a larger percentage of the population.Neutral mutations are defined as mutations whose effects do not influence the fitness of an individual. These can accumulate over time due to genetic drift. It is believed that the overwhelming majority of mutations have no significant effect on an organism's fitness. Also, DNA repair mechanisms are able to mend most changes before they become permanent mutations, and many organisms have mechanisms for eliminating otherwise permanently mutated somatic cells.Mutation is generally accepted by biologists as the mechanism by which natural selection acts, generating advantageous new traits that survive and multiply in offspring as well as disadvantageous traits, in less fit offspring, that tend to die out.Contents[hide] 1 Classification of mutation types 1.1 By effect on structure1.2 By effect on function1.3 By effect on fitness1.4 By inheritance 1.4.1 By pattern of inheritance1.5 By impact on protein sequence1.6 Special classes1.7 Causes of mutation1.8 Nomenclature2 Harmful mutations3 Beneficial mutations4 Prion mutation5 See also6 References7 External linksClassification of mutation typesIllustrations of five types of chromosomal mutations. Selection of disease-causing mutations, in a standard table of the genetic code of amino acids.[24]By effect on structureThe sequence of a gene can be altered in a number of ways. Gene mutations have varying effects on health depending on where they occur and whether they alter the function of essential proteins. Mutations in the structure of genes can be classified as: Small-scale mutations, such as those affecting a small gene in one or a few nucleotides, including: Point mutations, often caused by chemicals or malfunction of DNA replication, exchange a single nucleotide for another[25]. These changes are classified as transitions or transversions[26]. Most common is the transition that exchanges a purine for a purine (A ↔ G) or a pyrimidine for a pyrimidine, (C ↔ T). A transition can be caused by nitrous acid, base mis-pairing, or mutagenic base analogs such as 5-bromo-2-deoxyuridine (BrdU). Less common is a transversion, which exchanges a purine for a pyrimidine or a pyrimidine for a purine (C/T ↔ A/G). An example of a transversion is adenine (A) being converted into a cytosine (C). A point mutation can be reversed by another point mutation, in which the nucleotide is changed back to its original state (true reversion) or by second-site reversion (a complementary mutation elsewhere that results in regained gene functionality). Point mutations that occur within the protein coding region of a gene may be classified into three kinds, depending upon what the erroneous codon codes for: Silent mutations: which code for the same amino acid.Missense mutations: which code for a different amino acid.Nonsense mutations: which code for a stop and can truncate the protein.Insertions add one or more extra nucleotides into the DNA. They are usually caused by transposable elements, or errors during replication of repeating elements (e.g. AT repeats[citation needed]). Insertions in the coding region of a gene may alter splicing of the mRNA (splice site mutation), or cause a shift in the reading frame (frameshift), both of which can significantly alter the gene product. Insertions can be reverted by excision of the transposable element.Deletions remove one or more nucleotides from the DNA. Like insertions, these mutations can alter the reading frame of the gene. They are generally irreversible: though exactly the same sequence might theoretically be restored by an insertion, transposable elements able to revert a very short deletion (say 1-2 bases) in any location are either highly unlikely to exist or do not exist at all. Note that a deletion is not the exact opposite of an insertion: the former is quite random while the latter consists of a specific sequence inserting at locations that are not entirely random or even quite narrowly defined.Large-scale mutations in chromosomal structure, including: Amplifications (or gene duplications) leading to multiple copies of all chromosomal regions, increasing the dosage of the genes located within them.Deletions of large chromosomal regions, leading to loss of the genes within those regions.Mutations whose effect is to juxtapose previously separate pieces of DNA, potentially bringing together separate genes to form functionally distinct fusion genes (e.g. bcr-abl). These include: Chromosomal translocations: interchange of genetic parts from nonhomologous chromosomes.Interstitial deletions: an intra-chromosomal deletion that removes a segment of DNA from a single chromosome, thereby apposing previously distant genes. For example, cells isolated from a human astrocytoma, a type of brain tumor, were found to have a chromosomal deletion removing sequences between the "fused in glioblastoma" (fig) gene and the receptor tyrosine kinase "ros", producing a fusion protein (FIG-ROS). The abnormal FIG-ROS fusion protein has constitutively active kinase activity that causes oncogenic transformation (a transformation from normal cells to cancer cells).Chromosomal inversions: reversing the orientation of a chromosomal segment.Loss of heterozygosity: loss of one allele, either by a deletion or recombination event, in an organism that previously had two different alleles.By effect on functionLoss-of-function mutations are the result of gene product having less or no function. When the allele has a complete loss of function (null allele) it is often called an amorphic mutation. Phenotypes associated with such mutations are most often recessive. Exceptions are when the organism is haploid, or when the reduced dosage of a normal gene product is not enough for a normal phenotype (this is called haploinsufficiency).Gain-of-function mutations change the gene product such that it gains a new and abnormal function. These mutations usually have dominant phenotypes. Often called a neomorphic mutation.Dominant negative mutations (also called antimorphic mutations) have an altered gene product that acts antagonistically to the wild-type allele. These mutations usually result in an altered molecular function (often inactive) and are characterised by a dominant or semi-dominant phenotype. In humans, Marfan syndrome is an example of a dominant negative mutation occurring in an autosomal dominant disease. In this condition, the defective glycoprotein product of the fibrillin gene (FBN1) antagonizes the product of the normal allele.Lethal mutations are mutations that lead to the death of the organisms which carry the mutations.A back mutation or reversion is a point mutation that restores the original sequence and hence the original phenotype.[27]By effect on fitnessIn applied genetics it is usual to speak of mutations as either harmful or beneficial. A harmful mutation is a mutation that decreases the fitness of the organism.A beneficial mutation is a mutation that increases fitness of the organism, or which promotes traits that are desirable.In theoretical population genetics, it is more usual to speak of such mutations as deleterious or advantageous. In the neutral theory of molecular evolution, genetic drift is the basis for most variation at the molecular level.A neutral mutation has no harmful or beneficial effect on the organism. Such mutations occur at a steady rate, forming the basis for the molecular clock.A deleterious mutation has a negative effect on the phenotype, and thus decreases the fitness of the organism.An advantageous mutation has a positive effect on the phenotype, and thus increases the fitness of the organism.A nearly neutral mutation is a mutation that may be slightly deleterious or advantageous, although most nearly neutral mutations are slightly deleterious.By inheritanceinheritable generic in pro-generic tissue or cells on path to be changed to gametes.non inheritable somatic (eg, carcinogenic mutation)non inheritable post mortem aDNA mutation in decaying remains.By pattern of inheritanceThe human genome contains two copies of each gene - a paternal and a maternal allele. A heterozygous mutation is a mutation of only one allele.A homozygous mutation is an identical mutation of both the paternal and maternal alleles.Compound heterozygous mutations or a genetic compound comprises two different mutations in the paternal and maternal alleles.[28]A wildtype or homozygous non-mutated organism is one in which neither allele is mutated. (Just not a mutation)By impact on protein sequenceA frameshift mutation is a mutation caused by insertion or deletion of a number of nucleotides that is not evenly divisible by three from a DNA sequence. Due to the triplet nature of gene expression by codons, the insertion or deletion can disrupt the reading frame, or the grouping of the codons, resulting in a completely different translation from the original. The earlier in the sequence the deletion or insertion occurs, the more altered the protein produced is.A nonsense mutation is a point mutation in a sequence of DNA that results in a premature stop codon, or a nonsense codon in the transcribed mRNA, and possibly a truncated, and often nonfunctional protein product.Missense mutations or nonsynonymous mutations are types of point mutations where a single nucleotide is changed to cause substitution of a different amino acid. This in turn can render the resulting protein nonfunctional. Such mutations are responsible for diseases such as Epidermolysis bullosa, sickle-cell disease, and SOD1 mediated ALS (Boillée 2006, p. 39).A neutral mutation is a mutation that occurs in an amino acid codon which results in the use of a different, but chemically similar, amino acid. The similarity between the two is enough that little or no change is often rendered in the protein. For example, a change from AAA to AGA will encode lysine, a chemically similar molecule to the intended arginine.Silent mutations are mutations that do not result in a change to the amino acid sequence of a protein. They may occur in a region that does not code for a protein, or they may occur within a codon in a manner that does not alter the final amino acid sequence. The phrase silent mutation is often used interchangeably with the phrase synonymous mutation; however, synonymous mutations are a subcategory of the former, occurring only within exons. The name silent could be a misnomer. For example, a silent mutation in the exon/intron border may lead to alternative splicing by changing the splice site (see Splice site mutation), thereby leading to a changed protein.Special classesConditional mutation is a mutation that has wild-type (or less severe) phenotype under certain "permissive" environmental conditions and a mutant phenotype under certain "restrictive" conditions. For example, a temperature-sensitive mutation can cause cell death at high temperature (restrictive condition), but might have no deleterious consequences at a lower temperature (permissive condition).Causes of mutationTwo classes of mutations are spontaneous mutations (molecular decay) and induced mutations caused by mutagens. Spontaneous mutations on the molecular level include:Tautomerism - A base is changed by the repositioning of a hydrogen atom, altering the hydrogen bonding pattern of that base resulting in incorrect base pairing during replication.Depurination - Loss of a purine base (A or G) to form an apurinic site (AP site).Deamination - Hydrolysis changes a normal base to an atypical base containing a keto group in place of the original amine group. Examples include C → U and A → HX (hypoxanthine), which can be corrected by DNA repair mechanisms; and 5MeC (5-methylcytosine) → T, which is less likely to be detected as a mutation because thymine is a normal DNA base.Transition - A purine changes to another purine, or a pyrimidine to a pyrimidine.Transversion - A purine becomes a pyrimidine, or vice versa.A covalent adduct between benzo[a]pyrene, the major mutagen in tobacco smoke, and DNA[29] Induced mutations on the molecular level can be caused by:Chemicals Hydroxylamine NH2OHBase analogs (e.g. BrdU)Alkylating agents (e.g. N-ethyl-N-nitrosourea) These agents can mutate both replicating and non-replicating DNA. In contrast, a base analog can only mutate the DNA when the analog is incorporated in replicating the DNA. Each of these classes of chemical mutagens has certain effects that then lead to transitions, transversions, or deletions.Agents that form DNA adducts (e.g. ochratoxin A metabolites)[30]DNA intercalating agents (e.g. ethidium bromide)DNA crosslinkersOxidative damageNitrous acid converts amine groups on A and C to diazo groups, altering their hydrogen bonding patterns which leads to incorrect base pairing during replication.Radiation Ultraviolet radiation (nonionizing radiation). Two nucleotide bases in DNA - cytosine and thymine - are most vulnerable to radiation that can change their properties. UV light can induce adjacent thymine bases in a DNA strand to pair with each other, as a bulky dimer.Ionizing radiationViral infections[31]DNA has so-called hotspots, where mutations occur up to 100 times more frequently than the normal mutation rate. A hotspot can be at an unusual base, e.g., 5-methylcytosine.Mutation rates also vary across species. Evolutionary biologists have theorized that higher mutation rates are beneficial in some situations, because they allow organisms to evolve and therefore adapt more quickly to their environments. For example, repeated exposure of bacteria to antibiotics, and selection of resistant mutants, can result in the selection of bacteria that have a much higher mutation rate than the original population (mutator strains).NomenclatureNomenclature of mutations specify the type of mutation and base or amino acid changes. Nucleotide substitution (e.g. 76A>T) - The number is the position of the nucleotide from the 5' end, the first letter represents the wild type nucleotide, and the second letter represents the nucleotide which replaced the wild type. In the given example, the adenine at the 76th position was replaced by a thymine. If it becomes necessary to differentiate between mutations in genomic DNA, mitochondrial DNA, and RNA, a simple convention is used. For example, if the 100th base of a nucleotide sequence mutated from G to C, then it would be written as g.100G>C if the mutation occurred in genomic DNA, m.100G>C if the mutation occurred in mitochondrial DNA, or r.100g>c if the mutation occurred in RNA. Note that for mutations in RNA, the nucleotide code is written in lower case.Amino acid substitution (e.g. D111E) - The first letter is the one letter code of the wild type amino acid, the number is the position of the amino acid from the N terminus, and the second letter is the one letter code of the amino acid present in the mutation. Nonsense mutations are represented with an X for the second amino acid (e.g. D111X).Amino acid deletion (e.g. ΔF508) - The Greek letter Δ (delta) indicates a deletion. The letter refers to the amino acid present in the wild type and the number is the position from the N terminus of the amino acid were it to be present as in the wild type.Harmful mutationsChanges in DNA caused by mutation can cause errors in protein sequence, creating partially or completely non-functional proteins. To function correctly, each cell depends on thousands of proteins to function in the right places at the right times. When a mutation alters a protein that plays a critical role in the body, a medical condition can result. A condition caused by mutations in one or more genes is called a genetic disorder. Some mutations alter a gene's DNA base sequence but do not change the function of the protein made by the gene. Studies of the fly Drosophila melanogaster suggest that if a mutation does change a protein, this will probably be harmful, with about 70 percent of these mutations having damaging effects, and the remainder being either neutral or weakly beneficial.[32] However, studies in yeast have shown that only 7% of mutations that are not in genes are harmful.[33] If a mutation is present in a germ cell, it can give rise to offspring that carries the mutation in all of its cells. This is the case in hereditary diseases. On the other hand, a mutation may occur in a somatic cell of an organism. Such mutations will be present in all descendants of this cell within the same organism, and certain mutations can cause the cell to become malignant, and thus cause cancer[34].Often, gene mutations that could cause a genetic disorder are repaired by the DNA repair system of the cell. Each cell has a number of pathways through which enzymes recognize and repair mistakes in DNA. Because DNA can be damaged or mutated in many ways, the process of DNA repair is an important way in which the body protects itself from disease.Beneficial mutationsAlthough most mutations that change protein sequences are harmful, some mutations have a positive effect on an organism. In this case, the mutation may enable the mutant organism to withstand particular environmental stresses better than wild-type organisms, or reproduce more quickly. In these cases a mutation will tend to become more common in a population through natural selection. For example, a specific 32 base pair deletion in human CCR5 (CCR5-Δ32) confers HIV resistance to homozygotes and delays AIDS onset in heterozygotes.[35] The CCR5 mutation is more common in those of European descent. One possible explanation of the etiology of the relatively high frequency of CCR5-Δ32 in the European population is that it conferred resistance to the bubonic plague in mid-14th century Europe. People with this mutation were more likely to survive infection; thus its frequency in the population increased.[36] This theory could explain why this mutation is not found in Africa, where the bubonic plague never reached. A newer theory suggests that the selective pressure on the CCR5 Delta 32 mutation was caused by smallpox instead of the bubonic plague.[37]Prion mutationPrions are proteins and don't contain genetic material, however prion replication has been shown to be subject to mutationand natural selection just like other forms of replication.[38] See alsoAneuploidyAntioxidantBudgerigar colour geneticsHomeoboxMacromutationMuller's morphsMutantPolyploidyRobertsonian translocationSignature tagged mutagenesisSite-directed mutagenesisTILLING (molecular biology)References^ a b Bertram J (2000). "The molecular biology of cancer". Mol. Aspects Med. 21(6): 167-223. doi:10.1016/S0098-2997(00)00007-8. PMID 11173079.^ a b Aminetzach YT, Macpherson JM, Petrov DA (2005). "Pesticide resistance via transposition-mediated adaptive gene truncation in Drosophila". Science 309(5735): 764-7. doi:10.1126/science.1112699. PMID 16051794.^ Burrus V, Waldor M (2004). "Shaping bacterial genomes with integrative and conjugative elements". Res. Microbiol.155 (5): 376-86. doi:10.1016/j.resmic.2004.01.012. PMID 15207870.^ Sawyer SA, Parsch J, Zhang Z, Hartl DL (2007). "Prevalence of positive selection among nearly neutral amino acid replacements in Drosophila". Proc. Natl. Acad. Sci. U.S.A.104 (16): 6504-10. doi:10.1073/pnas.0701572104. PMID 17409186.^ Sniegowski P, Gerrish P, Johnson T, Shaver A (2000). "The evolution of mutation rates: separating causes from consequences". Bioessays 22 (12): 1057-66. doi:10.1002/1521-1878(200012)22:123.0.CO;2-W. PMID 11084621.^ Drake JW, Holland JJ (1999). "Mutation rates among RNA viruses". Proc. Natl. Acad. Sci. U.S.A. 96 (24): 13910-3. doi:10.1073/pnas.96.24.13910. PMID 10570172. PMC 24164. http://www.pnas.org/content/96/24/13910.long.^ Holland J, Spindler K, Horodyski F, Grabau E, Nichol S, VandePol S (1982). "Rapid evolution of RNA genomes". Science 215 (4540): 1577-85. doi:10.1126/science.7041255. PMID 7041255.^ Hastings, P J; Lupski, JR; Rosenberg, SM; Ira, G (2009). "Mechanisms of change in gene copy number". Nature Reviews. Genetics 10 (8): 551-564. doi:10.1038/nrg2593. PMID 19597530.^ Carroll SB, Grenier J, Weatherbee SD (2005). From DNA to Diversity: Molecular Genetics and the Evolution of Animal Design. Second Edition. Oxford: Blackwell Publishing. ISBN 1-4051-1950-0.^ Harrison P, Gerstein M (2002). "Studying genomes through the aeons: protein families, pseudogenes and proteome evolution". J Mol Biol 318 (5): 1155-74. doi:10.1016/S0022-2836(02)00109-2. PMID 12083509.^ Orengo CA, Thornton JM (2005). "Protein families and their evolution-a structural perspective". Annu. Rev. Biochem. 74: 867-900. doi:10.1146/annurev.biochem.74.082803.133029. PMID 15954844.^ Long M, Betrán E, Thornton K, Wang W (November 2003). "The origin of new genes: glimpses from the young and old". Nat. Rev. Genet. 4 (11): 865-75. doi:10.1038/nrg1204. PMID 14634634.^ Wang M, Caetano-Anollés G (2009). "The evolutionary mechanics of domain organization in proteomes and the rise of modularity in the protein world". Structure 17 (1): 66-78. doi:10.1016/j.str.2008.11.008. PMID 19141283.^ Bowmaker JK (1998). "Evolution of colour vision in vertebrates". Eye (London, England) 12 (Pt 3b): 541-7. PMID 9775215.^ Gregory TR, Hebert PD (1999). "The modulation of DNA content: proximate causes and ultimate consequences". Genome Res. 9 (4): 317-24. doi:10.1101/gr.9.4.317 (inactive 2009-11-14). PMID 10207154. http://genome.cshlp.org/content/9/4/317.full.^ Hurles M (July 2004). "Gene duplication: the genomic trade in spare parts". PLoS Biol. 2 (7): E206. doi:10.1371/journal.pbio.0020206. PMID 15252449.^ Liu N, Okamura K, Tyler DM (2008). "The evolution and functional diversification of animal microRNA genes". Cell Res. 18 (10): 985-96. doi:10.1038/cr.2008.278. PMID 18711447. PMC 2712117. http://www.nature.com/cr/journal/v18/n10/full/cr2008278a.html.^ Siepel A (October 2009). "Darwinian alchemy: Human genes from noncoding DNA". Genome Res. 19 (10): 1693-5. doi:10.1101/gr.098376.109. PMID 19797681. PMC 2765273. http://genome.cshlp.org/content/19/10/1693.full.^ Zhang J, Wang X, Podlaha O (2004). "Testing the chromosomal speciation hypothesis for humans and chimpanzees". Genome Res. 14 (5): 845-51. doi:10.1101/gr.1891104. PMID 15123584.^ Ayala FJ, Coluzzi M (2005). "Chromosome speciation: humans, Drosophila, and mosquitoes". Proc. Natl. Acad. Sci. U.S.A. 102 (Suppl 1): 6535-42. doi:10.1073/pnas.0501847102. PMID 15851677. PMC 1131864. http://www.pnas.org/content/102/suppl.1/6535.full.^ Hurst GD, Werren JH (2001). "The role of selfish genetic elements in eukaryotic evolution". Nat. Rev. Genet.2 (8): 597-606. doi:10.1038/35084545. PMID 11483984.^ Häsler J, Strub K (2006). "Alu elements as regulators of gene expression". Nucleic Acids Res. 34 (19): 5491-7. doi:10.1093/nar/gkl706. PMID 17020921.^ Eyre-Walker, A.; Keightley, P. (Aug 2007). "The distribution of fitness effects of new mutations". Nature reviews. Genetics 8 (8): 610-618. doi:10.1038/nrg2146. ISSN 1471-0056. PMID 17637733. edit^ References for the image are found in Wikimedia Commons page at: Commons:File:Notable mutations.svg#References.^ Freese, Ernst (April 1959). "The Difference between Spontaneous and Base-Analogue Induced Mutations of Phage T4". Proc. Natl. Acad. Sci. U.S.A. 45 (4): 622-33. doi:10.1073/pnas.45.4.622. PMID 16590424.^ Freese, Ernst (1959). "The Specific Mutagenic Effect of Base Analogues on Phage T4". J. Mol. Biol. 1: 87-105. doi:10.1016/S0022-2836(59)80038-3.^ Ellis NA, Ciocci S, German J (2001). "Back mutation can produce phenotype reversion in Bloom syndrome somatic cells". Hum Genet 108 (2): 167-73. doi:10.1007/s004390000447. PMID 11281456. http://link.springer.de/link/service/journals/00439/bibs/1108002/11080167.htm.^ Medterms.com^ Created from PDB 1JDG^ Pfohl-Leszkowicz A, Manderville RA (January 2007). "Ochratoxin A: An overview on toxicity and carcinogenicity in animals and humans". Mol Nutr Food Res 51 (1): 61-99. doi:10.1002/mnfr.200600137. PMID 17195275.^ Pilon L, Langelier Y, Royal A (1 August 1986). "Herpes simplex virus type 2 mutagenesis: characterization of mutants induced at the hprt locus of nonpermissive XC cells". Mol. Cell. Biol. 6 (8): 2977-83. PMID 3023954. PMC 367868. http://mcb.asm.org/cgi/pmidlookup?view=long&pmid=3023954.^ Sawyer SA, Parsch J, Zhang Z, Hartl DL (2007). "Prevalence of positive selection among nearly neutral amino acid replacements in Drosophila". Proc. Natl. Acad. Sci. U.S.A.104 (16): 6504-10. doi:10.1073/pnas.0701572104. PMID 17409186.^ Doniger SW, Kim HS, Swain D, et al. (August 2008). "A catalog of neutral and deleterious polymorphism in yeast". PLoS Genet. 4 (8): e1000183. doi:10.1371/journal.pgen.1000183. PMID 18769710.^ Ionov Y, Peinado MA, Malkhosyan S, Shibata D, Perucho M (1993). "Ubiquitous somatic mutations in simple repeated sequences reveal a new mechanism for colonic carcinogenesis". Nature 363 (6429): 558-61. doi:10.1038/363558a0. PMID 8505985.^ "CCR5 receptor gene and HIV infection, Antonio Pacheco.". http://www.cdc.gov/genomics/hugenet/factsheets/FS_CCR5.htm.^ "PBS:Secrets of the Dead. Case File: Mystery of the Black Death". http://www.pbs.org/wnet/secrets/previous_seasons/case_plague/clues.html.^ Galvani A, Slatkin M (2003). "Evaluating plague and smallpox as historical selective pressures for the CCR5-Δ32 HIV-resistance allele". Proc Natl Acad Sci USA 100(25): 15276-9. doi:10.1073/pnas.2435085100. PMID 14645720.^ 'Lifeless' prion proteins are 'capable of evolution'External links"All About Mutations" from the Huntington's Disease Outreach Project for Education at StanfordCentral Locus Specific Variation Database at the Institute of Genomics and Integrative BiologyThe mutations chapter of the WikiBooks General Biology textbookExamples of Beneficial MutationsCorrecting mutation by gene therapyBBC Radio 4 In Our Time - GENETIC MUTATION - with Steve Jones - streaming audio

What do you need for a axolotl?

Axolotl FactsPronounced: ACK-suh-LAH-tuhlOrigin: Mexico CityAlbino: Origin Reared in captivityTemperature: Keep in Unheated Aquarium 50-68F *No higherAttitude: Frequent biter of tank matesIssues: Will eat gravelSecurity: None neededFoods: worms, insect larva, crustaceans, fish, cricketsSupplements: None neededHousing: At least a gallon of water per axolotlWater: Clean water preferably hardIntroduction to AxolotlsThe Axolotl is very unique. The axolotl is a type of salamander, native to Mexico. It's scientific name is Ambystoma mexicanum. The common pet or laboratory Axolotl refers exclusively to A. mexicanum, although in Mexico the term Axolotl is used in reference to several species of Ambystoma, and is considered an edible food source.The Axolotl is neotenic, meaning that it doesn't routinely undergo metamorphosis from the larval to adult form, as happens with most other salamanders. Instead, the larval form (with gills) becomes sexually mature and reproduces, maintaining a strictly aquatic life style. Under some circumstances, the Axolotl can undergo metamorphosis into a terrestrial from, although this can be stressful on the animal.The Axolotl has amazing regenerative abilities- if injured, even to the point of losing a body part, the Axolotl will heal readily and even regenerate lost bits. Because Axolotls have the ability to regenerate lost body parts, axolotls are probably one of the most scientifically studied for this reason. They are fairly hardy creatures that can be expected to live up to 10-15 years with attention to proper care, particularly with respect ot water quality. Can grow up to 12 inches. Weight is from 2 to 8 oz. Their skin and gills are very sensitive and quite soft, so handling is not recommended any more than is necessary. Because they can exchange air through moist skin, they can survive outside of water for short periods, as long as their skin is not allowed to dry out.Juvenile axolotls can be cannibalistic towards each other, so they are best raised in separate enclosures. Adults can potentially be housed together but watch for cannibalistic tendencies. Of course, if a body part gets bitten off by a tank mate, an axolotl can regenerate it over time.Buy, For Sale, Selling, Price, Purchase, Cost, Sale, at; Axolotls Care Facts Axolotls (ambystoma mexicanum) Axolotls should not share their living space with other animals especially fish smaller than the mouth of the Axolotl will eat them. Also the fish will go after the axolotl's external gills. Axolotls 16 months and older Axolotls can live with other Axolotls because their cannibalistic phase should be over. TEMPERTURE The temperature of the aquarium is very important should be between 57 to 68 degrees Fahrenheit. Lower temperatures result in slow moving salamanders with slower metabolism, while higher temperatures than 68 causes stress. Too warm and the axolotl will die. If it is too cold this will only slow their metabolism. HOUSING Axolotls are entirely aquatic under normal circumstances and so fish tanks are the ideal home. But give your Axolotl enough room to move around. So an adult Axolotl should be kept in an aquarium at least 20 inches in length. Larger or more numerous Axolotls require larger tanks. The Axolotl's tank should have about 6 to 10 inches of water in it. Filters are essential as Axolotls produce a lot of waste. However Axolotls will eat gravel in the tank so it is a good idea to use no gravel or to use smooth rocks that are lager than the size of the Axolotl mouth. The water should be calm. They enjoy having plants, caves, and other decorations to hide in. WATER Water quality as essential for keeping bacteria low in your tank so it is recommended that you do 20 % of the water change should be done once a week. Taking time required to do water changes each week will greatly extend the life of your Axolotls. You should keep the water flow at a minimum because the water current can cause your Axolotls to be stressed from fighting the current. You will see that the Axolotl spend most of the time in the same spot, moving their gills occasionally to disperse carbon dioxide and circulate new oxygen. The water in the Axolotl's aquarium should have a pH of between 6.5 and 8. It should be free of chlorine. Axolotls prefer relatively hard water. If the tap water available is soft, it can be supplemented with added salts such as Holtfreter's and Steinberg's solutions. LIGHTING Axolotls have a low light requirement so the lighting should be fluorescent light with a low wattage lamp. Don't use bright lights or lights that generate any heat. Axolotl's eyes have no eyelids to protect them. FEEDING In their native habitat, axolotls eat the abundant small fauna, including snails, worms, and crustaceans, various small invertebrates such as daphnia, and small fish and amphibian. They will in fact eat just about anything that will fit into their mouth, but this doesn't mean they should. Generally they can be fed beef heart and other frozen or fresh carnivore's foods. Special axolotl food is also available. Avoid feeding them mince or other budget meats as they cannot tolerate fats. Any food that the axolotl doesn't eat should be removed after 24 hours otherwise it will begin to go rotten and spoil the water quality. Similarly any solid waste material should also be removed. If your axolotl is not eating be sure to check the water quality and temperature. GENERAL Axolotls are unique and easy to keep. Providing you maintain their water conditions they can live for up to 15 years and make an excellent pet and companion, no biting and no claws that can hurt. I you are in the USA, Axolotls can only be purchased within the United States. For additional information please look at my Bio Page. ====== ======

What are some of the behaviors of the axolotl?

Axolotls are carniverous and native to only one place in the entire world (Lake Xochimilco, Mexico), they also have both gills and lungs. The axolotl can grow from 15 to 45 centimeters but most commonly they stop growing at 23 cm. They are on the Critically Endangered list and are of the kingdom Animalia, phylum Chordata, class Amphibia, order Caudata, family Ambystomatidae, Genus Ambystoma, scientific name Ambystoma mexicanum. In Japan the axolotl is called the Wooper Rooper, and is often called the Mexican Mole Lizard in other parts of the world. Axolotls are cold blooded and typically live in a 10 gallon (38 l, 8.3 imp gal) tank with about 5.1 fl oz of water inside it.Axolotls live at temperatures of 14–20°C, higher temperature are considered to be harmful to the Axolotls. The Axolotl will spend a majority of the time on the bottom of a tank (floating is a sign of stress and illness).Australians and New Zealanders frequently refer to the Axolotl as the Mexican Walking Fish, though the Axolotl is not a fish but an amphibian, a salamander, part of the order Caudata/Urodela. Because it's a salamander, it's part of one of the three branches of class Amphibia, which also includes the frogs and toads (the Anurans), and the mainly eel-like order, Gymnophiona, which are also known as the Caecilians. Have a look at the Biology Page for a short guide to the Axolotl's body and characteristics. One common misconception is that axolotls and other salamanders are lizards or reptiles. In fact, amphibians are a completely separate group of animals. For example, did you know that reptiles and human beings have a four-chambered heart? Well amphibians have only three chambers. That's just one example of how appearance can be deceiving: salamanders might look like lizards, but they are very different indeed.This page is a brief introduction for those new to the Axolotl and salamanders. If you require specific information, you can search this site using the search facility at the top right of this page. Caudata.org also contains a wealth of axolotl information and it's a great place to buy axolotls or trade with other hobbyists. Caudata.org is the Internet's premier source of salamander and newt information and it places an emphasis on their maintenance in captivity. There is a very busy axolotl forum at Caudata.org, used by people just like you. I hope that you find this site useful, but most of all I hope you enjoy what you read and find here. If you're looking for information about metamorphosed axolotls, click here.Axolotls of various colours occur in captivity, including grey, shades of brown, leucistic (white with black eyes), golden albino, white albino, as well as other varieties, such as the melanoid (a near-black animal). The normally coloured axolotl, the "wild type", can be near-black like the one in the group photo to the left, chocolate brown like the one in the site's logo, or even creamy in colour, and anywhere in between. There are even "piebald" axolotls in various colours, and a variety that is piebald in more than one colour, known as the "harlequin". You can learn more about how colour comes about and how it is passed on by taking a look at the Genetics Page. And why not take a look at the hundreds of photos of the weird and wonderful varieties of axolotls submitted by enthusiasts like yourself at the Axolotl Section of the Caudata.org User Photo Galleries?The name "Axolotl" comes from the Aztec language, "Nahuatl". One of the most popular translations of the name connects the Axolotl to the god of deformations and death, Xolotl, while the most commonly accepted translation is "water-dog" (from "atl" for water, and "xolotl", which can also mean dog).Prior to the growth of Mexico city in the basin of Mexico, the Axolotl was native to both Lake Xochimilco, and Lake Chalco. Of these two high altitude freshwater lakes, only the remnants of Xochimilco as canals can be seen today. Unfortunately many information sources mention these lakes as if they still exist (such as this ill-researched article about a metamorphosed axolotl on the BBC News Web site). If only this were still the case: sadly it is rarely caught in the wild but at least the Axolotl is now on the CITES endangered species list. There have been efforts to breed and release the animal, in order to re-establish its numbers. However the location of the remaining waterways where the animal may live (located in the Mexico City metropolitan area) are likely to be very threatened by the city's continuing expansion and the days of the species surviving in the wild are surely quite limited. Fortunately, due to the importance of the Axolotl in scientific research, it is unheard of for them to be taken from the wild for that purpose because of the huge numbers bred in captivity each year. There are related Mexican Ambystoma species that also remain gilled as adults. These species are located in water bodies further from Mexico city and may have a slightly brighter future in the wild than the Axolotl.Despite its endangered status, the use of the Axolotl as a laboratory animal should ensure the species' survival, if only in captivity. It has long been known that the Axolotl is a worthy study due to its amazing healing and regeneration abilities. Normal wound healing in animals occurs through the growth of scar tissue, which is not the same as the original tissue, nor is it as robust. Normal wound healing also does not allow for most animals to re-grow a lost limb. However the axolotl is fully capable of complete limb re-growth. The animal has the added scientific attraction of having especially large embryos, making it easier to deal with under laboratory conditions. Its embryo is also very robust, and can be spliced and combined with different parts of other axolotl embryos with a high degree of success.The Axolotl is a fascinating creature for a number of reasons, including its grotesque appearance, its ability to regenerate, and primarily the fact that it exhibits the phenomenon known as neoteny. Ordinarily, amphibians undergo metamorphosis from egg to larva (the tadpole of a frog is a larva), and finally to adult form. The Axolotl, along with a number of other amphibians, remains in its larval form throughout its life. This means that it retains its gills and fins, and it doesn't develop the protruding eyes, eyelids and characteristics of other adult salamanders. It grows much larger than a normal larval salamander, and it reaches sexual maturity in this larval stage. Another term to describe this state is "perennibranchiate". The animal is completely aquatic, and although it does possess rudimentary lungs, it breathes primarily through its gills and to a lesser extent, its skin.It is generally accepted that neoteny is a "backward" step in evolution, because the Axolotl is descended from what were once terrestrial salamanders, like the closely related species, the Tiger Salamander, Ambystoma tigrinum and Ambystoma mavortium spp. (in fact, one likely theory suggests that the Axolotl is in fact a Tiger salamander off-shoot, as it can interbreed with that species with some success). Through some quirk of nature, a neotenous form developed and, probably due to environmental conditions, prospered. Neoteny is sometimes found in other amphibians, but tends to be caused by low levels of iodine (an essential element for animals to make thyroxine hormones, necessary for growth and development), or possibly by random genetic mutation. Research has also shown that very low temperatures can suppress the production of these hormones, thus also inducing neoteny.In the Axolotl, neoteny is now totally genetic (click for more information on the Axolotl's genetics). When treated with hormones, the axolotl will usually begin to metamorphose, but in very rare cases it will metamorphose spontaneously, such as the metamorphosed wild type axolotl pictured here. The metamorphosed wild type axolotl bears a close resemblance to the Mexican race of the Tiger Salamander, Ambystoma velasci. There is a wonderful thread on the Caudata.org forum here about the metamorphosed axolotl in the photo.The axolotl (pronounced /ˈæksəlɒtəl/), Ambystoma mexicanum, is a neotenic mole salamander belonging to the Tiger Salamander complex.[citation needed] Larvae of this species fail to undergo metamorphosis, so the adults remain aquatic and gilled. The species originates from the lake underlying Mexico City and is also called ajolote (which is also the common name for the Mexican Mole Lizard). Axolotls are used extensively in scientific research due to their ability to regenerate most body parts, ease of breeding, and large embryos. They are commonly kept as pets in the United States, Great Britain, Australia, Japan (sold under the name wooper looper (ウーパールーパー, Ūpā Rūpā?)) and other countries.[citation needed]Axolotls should not be confused with waterdogs, the larval stage of the closely related Tiger Salamanders (Ambystoma tigrinumand Ambystoma mavortium), which are widespread in much of North America and also occasionally become neotenic, nor with mudpuppies (Necturus spp.), fully-aquatic salamanders which are not closely related to the axolotl but bear a superficial resemblance.[citation needed]As of 2010[update], wild axolotls are near extinction[1] due to urbanization in Mexico City and polluted waters. Nonnative fish such as African tilapia and Asian carp have also recently been introduced to the waters. These new fish have been eating the axolotls' young, as well as its primary source of food.[2] The axolotl is currently on the International Union for Conservation of Nature's annual Red List of threatened species.[3]Contents[hide] 1 Description2 Habitat and ecology3 Axolotl's neoteny4 Use as a model organism5 Captivity6 See also7 References8 External linksDescriptionAdult axolotl. A sexually mature adult axolotl, at age 18--24 months, ranges in length from 15--45 cm (6--18 in), although a size close to 23 cm (9 in) is most common and greater than 30 cm (12 in) is rare. Axolotls possess features typical of salamander larvae, including external gills and a caudal fin extending from behind the head to the vent.[citation needed] Their heads are wide, and their eyes are lidless. Their limbs are underdeveloped and possess long, thin digits. Males are identified by their swollen cloacae lined with papillae, while females are noticeable for their wider bodies full of eggs. Three pairs of external gill stalks (rami) originate behind their heads and are used to move oxygenated water. The external gill rami are lined with filaments (fimbriae) to increase surface area for gas exchange.[citation needed] Four gill slits lined with gill rakers are hidden underneath the external gills. Axolotls have barely visible vestigial teeth, which would have developed during metamorphosis. The primary method of feeding is by suction, during which their rakers interlock to close the gill slits. External gills are used for respiration, although buccal pumping (gulping air from the surface) may also be used in order to provide oxygen to their lungs. Axolotls have four different colours, two naturally occurring colours and two mutants. The two naturally occurring colours are wildtype (varying shades of brown usually with spots) and melanoid (black). The two mutant colors are leucistic (pale pink with black eyes) and albino (golden, tan or pale pink with pink eyes).[citation needed]Habitat and ecologyThe axolotl is only native to Lake Xochimilco and Lake Chalco in central Mexico. Unfortunately for the axolotl, Lake Chalco no longer exists as it was artificially drained to avoid periodic flooding, and Lake Xochimilco remains a diminished glimpse of its former self, existing mainly as canals. The water temperature in Xochimilco rarely rises above 20 °C (68 °F), though it may fall to 6 or 7 °C (45 °F) in the winter, and perhaps lower. The wild population has been put under heavy pressure by the growth of Mexico City.[3] Axolotls are also sold as food in Mexican markets and were a staple in the Aztec diet.[2] They are currently listed by CITES as an endangered species and by IUCN as critically endangered in the wild, with a decreasing population. Axolotls are members of the Ambystoma tigrinum (Tiger salamander) complex, along with all other Mexican species of Ambystoma. Their habitat is like that of most neotenic species---a high altitude body of water surrounded by a risky terrestrial environment. These conditions are thought to favor neoteny. However, a terrestrial population of Mexican Tiger Salamanders occupies and breeds in the axolotl's habitat.The axolotl is carnivorous, consuming small prey such as worms, insects, and small fish in the wild. Axolotls locate food by smell, and will "snap" at any potential meal, sucking the food into their stomachs with vacuum force.[citation needed]Axolotl's neotenyAxolotls exhibit a property called neoteny, meaning that they reach sexual maturity without undergoing metamorphosis. Many species within the axolotl's genus are either entirely neotenic or have neotenic populations. In the axolotl, metamorphic failure is caused by a lack of thyroid stimulating hormone, which is used to induce the thyroid to produce thyroxine in transforming salamanders. The genes responsible for neoteny in laboratory animals may have been identified; however, they are not linked in wild populations, suggesting artificial selection is the cause of complete neoteny in laboratory and pet axolotls.[citation needed] Unlike some other neotenic salamanders (Sirens and Necturus), axolotls can be induced to metamorphose by an injection of iodine (used in the production of thyroid hormones) or by shots of thyroxine hormone. Another method for inducing transformation, though one that is very rarely successful, involves removing an axolotl in good condition to a shallow tank in a vivarium and slowly reducing the water level so that the axolotl has difficulty submerging.[citation needed] It will then, over a period of weeks, slowly metamorphose into an adult salamander. During transformation, the air in the vivarium must remain moist, and the maturing axolotl sprayed with a fine mist of pure water. The odds of the animal being able to metamorphose via this method are extremely small, and most attempts at inducing metamorphosis lead to death.[citation needed] This is likely due to the strong genetic basis for neoteny in laboratory and pet axolotls, which means that few captive animals have the ability to metamorphose on their own. Artificial metamorphosis also dramatically shortens the axolotl's lifespan if it survives the process. A neotenic axolotl will live an average of 10--15 years (though an individual in Paris is credited with achieving 25 years), while a metamorphosed specimen will scarcely live past the age of five. The adult form resembles a terrestrial Mexican Tiger Salamander, but has several differences, such as longer toes, which support its status as a separate species.[citation needed]Use as a model organismSee also: Model organism Six adult axolotls (including a leucistic specimen) were shipped from Mexico City to the Jardin des Plantes in Paris in 1863. Unaware of their neoteny, Auguste Duméril was surprised when, instead of the axolotl, he found in the vivarium a new species, similar to the salamander. This discovery was the starting point of research about neoteny. It is not certain that Mexican Tiger Salamanders were not included in the original shipment.Vilem Laufberger of Germany used thyroid hormone injections to induce an axolotl to grow into a terrestrial adult salamander. The experiment was repeated by the Englishman Julian Huxley, who was unaware the experiment had already been done, using ground thyroid hormones. Since then, experiments have been done often with injections of iodine or various thyroid hormones used to induce metamorphosis.[citation needed]Today, the axolotl is still used in research as a model organism, and large numbers are bred in captivity. Axolotls are especially easy to breed compared to other salamanders in their family, which are almost never captive bred due to the demands of terrestrial life. One attractive feature for research is the large and easily manipulated embryo, which allows viewing of the full development of a vertebrate. Axolotls are used in heart defect studies due to the presence of a mutant gene that causes heart failure in embryos. Since the embryos survive almost to hatching with no heart function, the defect is very observable. The presence of several colour morphs has also been extensively studied.[citation needed]The feature of the salamander that attracts most attention is its healing ability: the axolotl does not heal by scarring and is capable of the regeneration of entire lost appendages in a period of months, and, in certain cases, more vital structures. Some have indeed been found restoring the less vital parts of their brains. They can also readily accept transplants from other individuals, including eyes and parts of the brain---restoring these alien organs to full functionality. In some cases, axolotls have been known to repair a damaged limb as well as regenerating an additional one, ending up with an extra appendage that makes them attractive to pet owners as a novelty. In metamorphosed individuals, however, the ability to regenerate is greatly diminished. The axolotl is therefore used as a model for the development of limbs in vertebrates.[4]CaptivityAn axolotl in captivity Axolotls live at temperatures of 12 °C (54 °F)-20 °C (68 °F), preferably 17 °C (63 °F)-18 °C (64 °F). As for all poikilothermic organisms, lower temperatures result in slower metabolism; higher temperatures can lead to stress and increased appetite. Chlorine, commonly added to tapwater, is harmful to axolotls. A single typical axolotl typically requires a 40 l (11 US gal) tank with a water depth of at least 15 cm (6 in). Axolotls spend a majority of the time at the bottom of the tank.[citation needed]Salts, such as Holtfreter's solution, are usually added to the water to prevent infection.[5]In captivity, axolotls eat a variety of readily available foods, including trout and salmon pellets, frozen or live bloodworms, earthworms, and waxworms. Axolotls can also eat feeder fish, but care should be taken as fish left in the tank may graze on the axolotls' exposed gills.[citation needed]It should also be noted that Axolotls may suffer from impaction related issues if not kept on the correct substrate with fine sand being the preferred option. Impaction can be caused by the digestion of gravel and could be severe enough to cause death, therefore they must never be kept on gravel or stones that are smaller than the axolotls' head.The Mexican axolotl (pronounced ACK-suh-LAH-tuhl) salamander has the rare trait of retaining its larval features throughout its adult life. This condition, called neoteny, means it keeps its tadpole-like dorsal fin, which runs almost the length of its body, and its feathery external gills, which protrude from the back of its wide head.Found exclusively in the lake complex of Xochimilco (pronounced SO-chee-MILL-koh) near Mexico City, axolotls differ from most other salamanders in that they live permanently in water. In extremely rare cases, an axolotl will progress to maturity and emerge from the water, but by and large, they are content to stay on the bottom of Xochimilco's lakes and canals.Close relatives of the tiger salamander, axolotls can be quite large, reaching up to a foot (30 centimeters) in length, although the average size is closer to half that. They are typically black or mottled brown, but albino and white varieties are somewhat common, particularly among captive specimens.Axolotls are long-lived, surviving up to 15 years on a diet of mollusks, worms, insect larvae, crustaceans, and some fish. Accustomed to being a top predator in its habitat, this species has begun to suffer from the introduction of large fish into its lake habitat. Natural threats include predatory birds such as herons.Populations are in decline as the demands of nearby Mexico City have led to the draining and contamination of much of the waters of the Xochimilco Lake complex. They are also popular in the aquarium trade, and roasted axolotl is considered a delicacy in Mexico, further shrinking their numbers. They are considered a critically endangered species.By: GamerGalRox

All of the genes located on a given chromosome comprise a a karyotype b bridging cross c wild-type allele d linkage group e none of these?

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Allele that is the most common form of a gene in natural population or in a standard?

Is it true or false a control group must be present in an experiment?

What does cell autonomous mean?

Can give example about overdominance?

When daffodils grow wild are they pink?

What are some disadvantages for genetically engineered animals?

What is the results of a mutation?

What do you need for a axolotl?

What are some of the behaviors of the axolotl?

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