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A pseudogene is a gene that has been disabled by mutation, and is no longer functional.
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∙ 16y ago
Wiki User
∙ 14y agoare genes that have lost their ability to code for proteins so are no longer expressed in a cell.
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What is the difference between pseudogenes and duplicategenes?
Pseudogene is spelt P-s-e-u-d-o-g-e-n-e and duplicategene is spelt d-u-p-l-i-c-a-t-e-g-e-n-e.
What are introns and pseudogenes Are they the same?
Introns and pseudogenes are not the same.An intron is a segment of DNA that "intrudes" into or "interrupts" a coding stretch of DNA. Many genes in humans have introns, but bacteria seem to have none. To take an extreme example, the human dystrophin gene has 79 exons (separate coding segments) spread over more than 2.3 million base pairs.A pseudogene is a DNA segment that resembles a functional (coding) gene, but does not itself code for a gene product. It seems likely that pseudogenes arise when a gene is copied within the genome, and one of the copies drifts away from the functional sequence. "Pseudogene" literally means "false gene".
How psuedogenes contributed to evolutionary theory?
These genes have lost there protein coding abilities and are riddled with deleterious mutations. Two points to the evolutionary theory contribution. By example. Firstly, all great apes have a vitamin C pseudogene that links humans to all other great apes showing common ancestry. Secondly, this gene is inactive in fruitavores ( humans are common ancestors to fruitavores ) as they eat all the vitamin C they need so this gene became invisible to natural selection and deleterious mutation accumulating in the gene were not selected against as the survival and reproductive success of these organisms was no longer affected by not synthesizing vitamin C.
What is your stand on the evolutionary theory that men came from apes?
It is clear and obvious than men and ape share common ancestry. The skeletal features alone are sufficient to warrant this as a likely conclusion. But when we compare blood, tissue, and chromosomes, we are inexorably left with the realization our species diverged within the past ten million years, and the fossil evidence also bears this out. Humans have 23 pairs of chromosomes, whereas most other primates have 24 pairs (I'm not certain about lemurs, lorises, or tarsiers). However, it has been demonstrated that our reduced chromosome count stems from the fusion of a pair of early hominid chromosomes. We see tale-tell signs of the fusion by the presence of telomeres, repeated DNA segments near the ends of chromosomes, where the fusion occurred. Suppose you created monkeys, and then later created men. Why would you endow each with the same defect? Monkeys and humans both share a pseudogene for expressing a protein that synthesizes ascorbic acid. In each of us the gene does not function, which is why it is called a "pseudogene." Most other species of mammals have a functioning gene, so their diets need not be rich in vitamin C to ensure their good health. We suffer scurvy if we don't get it. We engineered mice with the human pseudogene in place of their GULO gene. These mice all developed classic symptoms of scurvy when fed diets restricted of ascorbic acid (vitamin C). This proves we correctly identified both the gene and its function. Separate creations? What possible explanation could there be for designing the same flaw into our respective species? That makes zero sense. However, if we imagine the gene breaking and becoming fixed in an arboreal population rich in vitamin C where the missing gene would go unnoticed, common ancestry explains the presence of the gene in both populations beautifully. Yet more evidence for common ancestry stems from comparisons of mitochondrial DNA. Mitochondria are organelles within cells that have their own DNA. These are inherited in the egg of the mother, the male sperm does not pass on its own mitochondria. We have grown cows with the mitochondria of rabbits, showing that dramatically unrelated species function just fine with foreign mtDNA (mitochondrial DNA). The mtDNA of chimps and humans is remarkably similar, again indicating our divergence was likely fairly recent in geologic time.
What animal cannot synthesize vitamin C?
Humans are not able to synthesize Vitamin C thus we are able to take up a lot in our diet.Every winter, as the influenza (flu) season spreads across America, people flock to stores to get vitamin C tablets to deliver them from the symptoms of the common cold. Vitamin C, or ascorbic acid, is an important cofactor that stimulates the immune system and apparently assists in shortening the length of illness and the severity of flu symptoms (although the exact effects of vitamin C on the flu are still debated). In addition to stimulating the immune system, vitamin C has been identified with several other functions in the human body including production of an important protein, collagen, found in several types of connective tissue including bone and cartilage (Garrett 1999). A deficiency in vitamin C can cause scurvy, a disease that results from deterioration of connective tissue, and prolonged lack of vitamin C can even lead to death (Marieb 1998). Humans are unable to synthesize vitamin C, but are able to store a 30-day supply of this important nutrient. To maintain this supply, a person must ingest about 60 mg of vitamin C each day, or approximately the amount of vitamin C in an average size orange. Although humans, apes, monkeys, fruit bats, and several species of fish (including trout and salmon) are unable to synthesize vitamin C, many other animals are quite capable of making their own vitamin C and do not need to eat fruit and vegetables to acquire this nutrient (Garrett 1999).Many people, especially in northern climates during the winter, have suffered from a lack of vitamin C throughout history. It's very likely that many people have died from scurvy as a result of being unable to provide themselves with fresh fruit and vegetables during the winter months. If vitamin C is such an important nutrient, and many other animals possess the ability to synthesize it, why didn't God give humans the biochemical pathways to synthesize vitamin C? There are two obvious possibilities why people today cannot synthesize vitamin C: (1) Humans were created without the ability to synthesize vitamin C, or (2) they lost the information from genes that code for the proteins necessary to synthesize vitamin C.The first possibility is very simple and there is logical Biblical and scientific support for this scenario. From the beginning, Adam and Eve were not created with a biochemical pathway for making vitamin C and were dependent on eating fruit, the best source of vitamin C. We know they were instructed to eat any fruit in the Garden of Eden except fruit from the Tree of the Knowledge of Good and Evil, and yet had access to the Tree of Life. Adam and Eve lived in an environment with many similarities to heaven. However, unlike those in heaven, Adam and Eve were commanded to be fruitful and multiply, and produce little Adams and Eves. Human reproduction would require nutrients to build tissues for the child during and after pregnancy, an indication that Adam and Eve had to eat to provide for their developing children and also for the maintenance of their own bodies. Furthermore, today nutritionists recommend a diet high in fruit and vegetables as being the healthiest source of nutrients, which is consistent with what God instructed Adam and Eve to eat. It is possible that God made Adam and Eve (and us) dependent on fruit as a source of vitamin C as a reminder that they were dependent on Him for food that must be eaten to stay healthy.Is it possible that Adam and Eve did have the information in their genes to produce the enzymes necessary for synthesizing vitamin C? Are there any remnants of those genes that can be identified in the human genome today? What would a non-functioning remnant of a gene look like if scientists found one? One thing is sure today -- if Adam and Eve did have the information in their genes to make vitamin C, health problems with scurvy recorded as far back as the Roman Empire (Davies 1970) indicate this information disappeared long ago from the human genome.There are sequences of DNA (in the genome) that are claimed to be nonfunctional remnants of presently functional genes. These sequences of DNA are called pseudogenes, and there are several criteria used to distinguish pseudogenes from functional genes. A pseudogene DNA sequence typically is greater than 70% similar (homologous) to a functional gene but lacks a promoter that would enable the sequence to be transcribed into RNA and finally a protein (Zhang et al. 2003). Pseudogenes also typically have disruptions to the "coding region," such as stop codons that prematurely end the translation of the gene into a protein (Zhang et al. 2003). Pseudogenes are believed to vary significantly from the original functioning gene because they are no longer under selective constraints. In other words, since the cell is no longer using this stretch of DNA, it accumulates mutations at a fast rate -- degrading the original functional gene sequence into a pseudogene (Karp 2002). Many pseudogenes are identified by comparing similar sequences in the genome to functional genes within an organism. For example, in humans there are many functional genes for ribosomal proteins, and there are several human ribosomal pseudogenes that meet the criteria mentioned above (Zhang et al. 2003). To find a pseudogene for vitamin C in the human genome, a comparison would have to be made between the human genome and the genome of an organism that had a functional gene for synthesizing vitamin C.In 1994, a group of Japanese scientists identified a DNA sequence in humans that had many similarities to the rat gene that codes for the enzyme (L-gulono-γ-lactone) that catalyzes the last step of vitamin C synthesis (Nishikimi et al. 1994). The human pseudogene sequence discovered has four of these 12 exons. (Exons are the modular coding regions of a gene.) These four human exon sequences have many characteristics of a pseudogene. There is a 70-80% sequence homology between the rat and human sequences depending on the exon, and two stop codons. Later analysis confirmed that these four exons are present in other primates as well (Inai, Ohta, and Nishikimi 2003). Humans are missing only the final enzyme for the last step in synthesizing vitamin C, but have all of the other enzymes necessary to convert glucose into vitamin C.It would seem from the evidence of a potential human pseudogene for L-gulono-γ-lactone and the presence of the other enzymes necessary for synthesizing vitamin C that humans have lost the ability to make vitamin C. However, there is more to this story. There are only four exons for the gene encoding L-gulono-γ-lactone in humans. Two-thirds of the homologous rat gene is completely missing. Most pseudogenes represent 90% of the entirefunctional gene. This DNA sequence, labeled as a pseudogene, might have an entirely different function than the rat gene.Stating that only the last enzyme is missing for the pathway to convert glucose to vitamin C might imply to the untrained individual that there is a biochemical pathway that leads to a dead end. Actually, the biochemical pathway that leads to the synthesis of vitamin C in rats also leads to the formation of five-carbon sugars in the pentose phosphate pathway present in virtually all animals (Linster and Van Schaftingen 2007). There are several metabolic intermediates in this pathway illustrating that these substances can be used as precursors for many compounds in the cell. In the pentose phosphate pathway, five-carbon sugars are made from glucose (a six-carbon sugar) to be used in the synthesis of DNA, RNA, and many energy producing substances such as ATP and NADPH (Garrett 1999). Animals that synthesize vitamin C can use both pathways illustrated in the simplified diagram below. Humans and the other animals "less fortunate" than rats only use the pentose phosphate pathway.There is no dead end or wasted metabolic intermediates, and there is no need to have the enzyme to make vitamin C since humans are able to get all of the vitamin C they need from food substances.Thousands of human pseudogenes have been catalogued, but in spite of the similarities to functional genes, the exact role of pseudogene sequences in the genome are not known by any scientist. It is not necessary to assume that pseudogenes are remnants of once functioning genes that have been lost and now clutter the genome like junk in a rubbish heap. It is possible that these regions of DNA do have a role in human and animal genomes and this role has not been discovered yet. Over 100 years ago, Robert Wiedersheim hypothesized that the human body had more than 80 organs that lacked any function simply because it was unknown at the time what these organs did (Wiedersheim 1895). They were assumed to be vestigial or "junk" leftovers from evolutionary history and several of these organs are still presented this way in biology textbooks today. The science of genomics is in the same position today. Just because scientists do not currently know the function of a portion of DNA does not mean that it does not have any function and therefore it is an evolutionary leftover. It has been reported that pseudogenes play a regulatory role in yeast for the functional genes that they share sequence homology with (Hirotsune et al. 2003). There needs to be more research in this area to verify these claims, but at least there are some indications of a functional role for pseudogenes in the human genome.So, did Adam and Eve have a gene to code for an enzyme that would synthesize vitamin C and was this information eventually lost as a result of the curse, or were they simply created without this information in their genomes? That question might not get answered until Christ returns. But in the meantime, humans require plenty of vitamin C in their diet -- so have an orange!
Explain how the reproductive adaptations of the platypus increases the chance of the continuity of the species in the Australian Environment?
because it is =P == Fertilization in the platypus exhibits both sauropsid and therian characteristics. Platypus ova are small (4 mm diameter) relative to comparably sized reptiles and birds, and eggs hatch at an early stage of development so that most growth of the embryo and infant is dependent on lactation, as in marsupials. Like all mammals and many other amniotes, when fertilization occurs the ovum is invested with a zona pellucida. The platypus genome encodes each of the four proteins of the human zona pellucida38, as well as two ZPAX genes (Table 1) that previously were observed only in birds, amphibians and fish. The aspartyl-protease nothepsin is present in platypus, but has been lost from marsupial and eutherian genomes (Table 1). In zebrafish, this gene is specifically expressed in the liver of females under the action of oestrogens, and accumulates in the ovary39. These are the same characteristics as of the vitellogenins, indicating that nothepsin may be involved in processing vitellogenin or other egg-yolk proteins. We find that platypus has retained a single vitellogenin gene and pseudogene, whereas sauropsids such as chicken have three and the viviparous marsupials and eutherians have none. == Orthologues of many of the eutherian sperm membrane proteins related to fertilization40 are present in platypus (and marsupial) genomes. These include the genes for a number of putative zona pellucida receptors and proteins implicated in sperm-oolemma fusion. Testis-specific proteases, which in eutherians participate in degradation of the zona pellucida during fertilization, are all absent from the platypus genome assembly. Monotreme spermatozoa undergo some post-testicular maturational changes, including the acquisition of progressive motility, loss of cytoplasmic droplets and aggregation of single spermatozoa into bundles during passage through the epididymis11. Nevertheless, maturational changes in the sperm surface that are both unique and essential in other mammals for fertilization of the ovum have yet to be identified. Also, the epididymis of monotremes is not highly adapted for sperm storage as in most marsupial and eutherian mammals. Consistent with these findings is the absence of platypus genes for the epididymal-specific proteins that have been implicated in sperm maturation and storage in other mammals. The most abundant secreted protein in the platypus epididymis is a lipocalin, the homologues of which are the most secreted proteins in the reptilian epididymis41. Notably, ADAM7, a protease that is secreted in the epididymis of eutherians, has an orthologue in the platypus. This is a bona fide protease with a characteristic Zn2+-coordinating sequence HExxH in the platypus, in the opossum and the tree shrew (Tupaia belangeri). However, loss of its proteolytic activity is predicted in eutherians42 owing to a single point mutation within its active site (E to Q). == Lactation is an ancient reproductive trait whose origin predates the origin of mammals. It has been proposed that early lactation evolved as a water source to protect porous parchment-shelled eggs from desiccation during incubation43 or as a protection against microbial infection. Parchment-shelled egg-laying monotremes also exhibit a more ancestral glandular mammary patch or areola without a nipple that may still possess roles in egg protection. However, in common with all mammals, the milk of monotremes has evolved beyond primitive egg protection into a true milk that is a rich secretion containing sugars, lipids and milk proteins with nutritional, anti-microbial and bioactive functions. In a reflection of this eutherian similarity platypus casein genes are tightly clustered together in the genome, as they are in other mammals, although platypus contains a recently duplicated -casein gene (Supplementary Fig. 2). Mammalian casein genes are thought to have originally arisen by duplication of either enamelin or ameloblastin44, both of which are tooth enamel matrix protein genes that are located adjacent to the casein gene cluster in eutherians and, we find, also in platypus. Adult platypuses, as well as echidnas, lack teeth but the conservation of these enamel protein genes is consistent with the presence of teeth and enamel in the juvenile, as well as the fossil platypuses45. because it is =P == Fertilization in the platypus exhibits both sauropsid and therian characteristics. Platypus ova are small (4 mm diameter) relative to comparably sized reptiles and birds, and eggs hatch at an early stage of development so that most growth of the embryo and infant is dependent on lactation, as in marsupials. Like all mammals and many other amniotes, when fertilization occurs the ovum is invested with a zona pellucida. The platypus genome encodes each of the four proteins of the human zona pellucida38, as well as two ZPAX genes (Table 1) that previously were observed only in birds, amphibians and fish. The aspartyl-protease nothepsin is present in platypus, but has been lost from marsupial and eutherian genomes (Table 1). In zebrafish, this gene is specifically expressed in the liver of females under the action of oestrogens, and accumulates in the ovary39. These are the same characteristics as of the vitellogenins, indicating that nothepsin may be involved in processing vitellogenin or other egg-yolk proteins. We find that platypus has retained a single vitellogenin gene and pseudogene, whereas sauropsids such as chicken have three and the viviparous marsupials and eutherians have none. == Orthologues of many of the eutherian sperm membrane proteins related to fertilization40 are present in platypus (and marsupial) genomes. These include the genes for a number of putative zona pellucida receptors and proteins implicated in sperm-oolemma fusion. Testis-specific proteases, which in eutherians participate in degradation of the zona pellucida during fertilization, are all absent from the platypus genome assembly. Monotreme spermatozoa undergo some post-testicular maturational changes, including the acquisition of progressive motility, loss of cytoplasmic droplets and aggregation of single spermatozoa into bundles during passage through the epididymis11. Nevertheless, maturational changes in the sperm surface that are both unique and essential in other mammals for fertilization of the ovum have yet to be identified. Also, the epididymis of monotremes is not highly adapted for sperm storage as in most marsupial and eutherian mammals. Consistent with these findings is the absence of platypus genes for the epididymal-specific proteins that have been implicated in sperm maturation and storage in other mammals. The most abundant secreted protein in the platypus epididymis is a lipocalin, the homologues of which are the most secreted proteins in the reptilian epididymis41. Notably, ADAM7, a protease that is secreted in the epididymis of eutherians, has an orthologue in the platypus. This is a bona fide protease with a characteristic Zn2+-coordinating sequence HExxH in the platypus, in the opossum and the tree shrew (Tupaia belangeri). However, loss of its proteolytic activity is predicted in eutherians42 owing to a single point mutation within its active site (E to Q). == Lactation is an ancient reproductive trait whose origin predates the origin of mammals. It has been proposed that early lactation evolved as a water source to protect porous parchment-shelled eggs from desiccation during incubation43 or as a protection against microbial infection. Parchment-shelled egg-laying monotremes also exhibit a more ancestral glandular mammary patch or areola without a nipple that may still possess roles in egg protection. However, in common with all mammals, the milk of monotremes has evolved beyond primitive egg protection into a true milk that is a rich secretion containing sugars, lipids and milk proteins with nutritional, anti-microbial and bioactive functions. In a reflection of this eutherian similarity platypus casein genes are tightly clustered together in the genome, as they are in other mammals, although platypus contains a recently duplicated -casein gene (Supplementary Fig. 2). Mammalian casein genes are thought to have originally arisen by duplication of either enamelin or ameloblastin44, both of which are tooth enamel matrix protein genes that are located adjacent to the casein gene cluster in eutherians and, we find, also in platypus. Adult platypuses, as well as echidnas, lack teeth but the conservation of these enamel protein genes is consistent with the presence of teeth and enamel in the juvenile, as well as the fossil platypuses45.
Another science word that starts with a P?
P element P1 P1-derived artificial chromosome P1-derived artificial chromosome (PAC) P53 PAC pachynema Paleontology palindrome Palindromic sequence pAMP Pan balance Panel testing panmictic papilla papillate paracentric inversion paralogous genes paramecin parameters parapatric speciation Parasegment border parasexual cycle parasite Parasitism Parasitology parasympathetic nervous system paratope parent generation parental ditype (PD) parenteral parietal lobes parthenogenesis partial digest particle particulate inheritance parts per billion (ppb) Parts per million (ppm) Pascal's triangle passive diffusion passive transport paternally path diagram pathogen pathogenesis pathogenic pathogenicity pathology pathovar patient patroclinous inheritance pattern formation pBR 322 pBR322 PCR PCR amplicons pedigree pelagic pellet Pelvic inflammatory disease (PID) penetrance pent- peptide peptide bond peptidyl site peptidyl transferase per- percent coefficient of variation percent concentration percent error percent yield peri- peri-natal pericentric inversion pericentromere perinatal period periodic law peripheral membrane protein peripheral nervous system (PNS) peripheral neurons peripheral neuropathy periphyton permissive condition permissive temperature peroxidase Persistence Pest sequence Pesticide petite petite mutation petrifaction pH pH scale phagocytes phagocytosis pharmacotyping pharyngeal arches pharynx phasmid Phencyclidine hydrochloride (PCP) phenocopy phenotype phenotypic sex determination phenotypic variance Phenylalanine phenylketonuria (pku) pheromone Philadelphia chromosome phloem Phosphatase Phosphate group phosphodiester bond phosphodiesterase Phospholipase A2 (PLA2) phospholipids Phosphorus (P) phosphorylate Phosphorylation photic zone photoautotroph photoheterotroph photon photoreactivation Photorespiration phragmospore phyletic gradualism phylloplane phylogenetic tree physical change physical chemistry Physical map phytoplankton phytoplasma phytotoxic phytotoxin piebald pilus (plural pili) Pipettes Pituitary pK pKa placebo placenta planet plankton plant plant breeding plaque plasma Plasma membrane plasmalemma plasmid plasmid suicide vector plasmogamy plasmolysis plastid plate platelet platelet-activating factor (PAF) Pleiotrophy pleiotropic mutation pleiotropy pleo- plerome plesionecrosis plexus ploidy Pluripotency PMA poikilothermal point mutation Poisson distribution poky mutation polar polar body polar covalent bond polar effect polar gene conversion polar granules polar molecule polar mutation polarity polarity gene Pole cells Pollen grain pollinator Poly(A) polymerase poly- poly-A tail poly-dA/poly-dT technique polyacrylamide Polyacrylamide gel electrophoresis polyadenosine tail polyatomic polycistronic polycistronic mRNA Polyclonal antibodies polydactyly polyethylene polygene polygenic Polygenic disorder polygenic inheritance polyinvagination islands Polylinker Polymer polymerase (DNA or RNA) polymerase chain reaction polymerase slippage polymerase slippage model polymerize polymodal polymorphism polynucleate Polynucleotide polynucleotide phosphorylase polynucleotide polymerase polyolefin polypeptide polyphenism polyphyletic polyploid polysaccharide polysome polyspermy polytene chromosome Polyvalent vaccine pons population population density Population genetics position effect position-effect variegation Positional cloning Positional information positive assortative mating positive control positive interference post- post-transcriptional modification posterior neuropore postmortem postreplicative repair Postsynaptic Membrane potential energy potentiometric titration pre- pre-mRNA pre-symptomatic pre-synaptic terminal precipitate precision precocious predation predator preemptor stem preformationism Premarket Approval prey Pribnow box Primary cell primary consumer primary oocyte primary spermatocyte primary structure primary transcript primase primer primitive folds primitive streak primosome prion prion rods pro-inflammatory cytokines probability probability theory probe Probe Amplification processivity producer product product of meiosis product rule proflavin progeny testing prokaryote prokaryotic cell prolepsis proliferate Proline promoter Pronucleus proofread prophage prophase proplastid propositus prosencephalon prostaglandins prostate gland protamine protease proteasome protein protein aggregate protein synthesis Proteolytic Proteome Proteomics proto-oncogene protocorm proton proton acceptor proton donor proton gradient protoplast protostomes prototroph provirus prox- proximal PrP pseudo- pseudoallele pseudoautosomal gene pseudodominance pseudogene pull down assays pull-down assays pulse-chase experiment pulsed-field gel electrophoresis punctuated equilibrium Punnett square pure pure-breeding line or strain purines Purkinje cells putamen pycnosis pygmism pyknosis pyramidal nerve cells pyriform pyrimidine pyruvate pyruvic acid
