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PubMed1991

Primate DRB6 pseudogenes: clue to the evolutionary origin of the HLA-DR2 haplotype.

The HLA-DR2 haplotype contains three beta-chain encoding DRB genes and one alpha-chain encoding DRA gene. Of the three DRB genes, two are presumably functional (HLA-DRB1 and HLA-DRB5), whereas the third (HLA-DRBVI) is a pseudogene. A pseudogene closely related to HLA-DRBVI is present in the chimpanzee (Patr-DRB6) and in the gorilla (Gogo-DRB6). We sequenced the HLA-DRBVI and Patr-DRB6 pseudogenes (all exons and most of the introns), and compared the sequence to that of the Gogo-DRB6 gene (of which only the exon sequence is available). All three pseudogenes seem to lack exon 1 and contain other deletions responsible for shifts in the translational reading frame. At least the HLA-DRBVI pseudogene, however, seems to be transcribed nevertheless. The chimpanzee pseudogene contains two inserts in intron 2, one of which is an Alu repeat belonging to the Sb subfamily, while the other remains unidentified. These inserts are lacking in the human gene. A comparison with sequences published by other investigators revealed the presence of the HLA-DRBVI pseudogene also in the DR1 and DRw10 haplotypes. Measurements of genetic distances indicate DRB6 to be closely related to the DRB2 pseudogene and to the HLA-DRB4 functional gene. In humans, gorillas, and chimpanzees, the DRB6 pseudogene is associated with the same functional gene (DRB5) indicating that this linkage disequilibrium is at least six million years old and that DR2 is one of the oldest DR haplotypes in higher primates.

Animals↗
PubMed1988

Characterization, evolutionary relationships, and chromosome location of processed mouse HPRT pseudogene.

Studies on a cell line with amplified copies of the mouse hypoxanthine-guanine phosphoribosyltransferase (HPRT) gene and HPRT gene transfer experiments revealed the existence of a nonfunctional HPRT-related sequence in the mouse genome. This sequence was isolated and found to be a processed HPRT pseudogene. With the exception of a small internal deletion, the pseudogene is believed to comprise a complete reverse transcript of HPRT mRNA, although the 3' end of the pseudogene was lost in the cloning process. A probe from a region flanking the mouse pseudogene was used to investigate the evolutionary relationships of mammalian HPRT pseudogenes. The pseudogenes in mouse and Chinese hamster appear to have a common origin, but no homology to any of the four known human HPRT pseudogenes was detected. A pseudogene-linked restriction fragment length polymorphism was used to map the pseudogene to the distal end of mouse chromosome 17.

Animals↗
PubMed1998

Comparative analysis of evolution in a rodent histone H2a pseudogene.

Sequences were obtained from five species of rodents that are orthologous to an H2a histone pseudogene from Mus musculus. The pseudogene is part of the cluster of replication-dependent histone genes found on Mus musculus chromosome 13. Comparative analysis of these five sequences together with the previously published sequence from M. musculus shows that this gene has likely been a pseudogene throughout the evolution of the genus Mus, while the gene from Rattus norvegicus is likely functional. Three large (> 20 bp) deletions were found among the Mus pseudogenes, a feature that is very unusual compared to surveys of processed pseudogenes. In addition, there are two single-base deletions and one 4-bp insertion among the Mus pseudogenes. The species distributions of one of the large deletions and the 4-bp insertion require either independent insertions of an identical sequence, independent deletions with identical boundaries, or a deletion followed by precise reintegration of the original sequence. The evidence favors the hypothesis of multiple deletions with identical boundaries. The "coding" regions of the Mus pseudogenes show a much reduced level of among-species variability in the 3' half of the pseudogene, compared both to the 5' half and to flanking sequences. This supports a hypothesis that the 3' end of the pseudogene is the target of frequent gene conversion by functional H2a genes.

Animals↗
PubMed2004

Gene rearrangements and evolution of tRNA pseudogenes in the mitochondrial genome of the parrotfish (Teleostei: Perciformes: Scaridae).

Genomic size of animal mitochondrial DNA is usually minimized over time. Thus, when regional duplications occur, they are followed by a rapid elimination of redundant material. In contrast to this general view, we report here long-sustained tRNA pseudogenes in the mitochondrial genome (mitogenome) of teleost fishes of the family Scaridae (parrotfishes). During the course of a molecular phylogenetic study of the suborder Labroidei, we determined the complete nucleotide sequence of the mitogenome for a parrotfish, Chlorurus sordidus, and found a gene rearrangement accompanied by a tRNA pseudogene. In the typical gene order of vertebrates, a tRNA-gene cluster between ND1 and ND2 genes includes tRNA(Ile) (I), tRNA(Gln) (Q), and tRNA(Met) (M) genes in this order (IQM). However, in the mitogenome of the parrotfish, the tRNA(Met) gene was inserted between the tRNA(Ile) and the tRNA(Gln) genes, and the tRNA(Gln) gene was followed by a putative tRNA(Met) pseudogene (psiM). Such a tRNA gene rearrangement including a pseudogene (IMQpsiM) was found in all of the 10 examined species, representing 7 of the 10 currently recognized scarid genera. All sister groups examined (20 species of Labridae and a single species of Odacidae) had the typical gene order of vertebrate mitogenomes. Phylogenetic analysis of the tRNA(Met) genes and the resulting pseudogenes demonstrated that the ancestral tRNA(Met) gene was duplicated in a common ancestor of the parrotfish. Based on the fossil record, these results indicate that the pseudogenes have survived at least 14 million years. Most of the vertebrate mitochondrial gene rearrangements involving the IQM region have held the tRNA(Met) gene just upstream of the ND2 gene, and even in a few exceptional cases, including the present ones, the tRNA pseudogenes have been found in that position. In addition, most of these tRNA(Met) pseudogenes maintained clover-leaf secondary structures, with the remainder sustaining the clover-leaf structure in the "top half (TpsiC and acceptor arms). Considering their potential secondary structures (holding "top halves" of the clover-leaf structures), locations within mitogenomes (flanking the 5' ends of the ND2 genes) and stabilities over time (survived at least 14 Myr), it is likely that the tRNA pseudogenes retain function as punctuation marks for mitochondrial ND2 mRNA processing.

Amino Acid Sequence↗
PubMed2004

Cloning of a kallikrein pseudogene.

OBJECTIVES: Kallikreins are a group of serine proteases clustered together on a small region of chromosome 19q13.4. Recent reports suggest that kallikreins are differentially expressed in malignancy and have potential as cancer biomarkers. The human kallikrein gene locus has now been fully characterized and 15 functional kallikreins were identified. Although many kallikrein pseudogenes have already been characterized in rodents, none have been identified in humans. METHODS AND RESULTS: In the current study, we identified the first human kallikrein pseudogene named PsiKLK1 and mapped it between the KLK2 and KLK4 genes. This pseudogene shares a moderate degree of similarity with the adjacent functional kallikreins. It has a conserved histidine residue of the catalytic triad of serine proteases and its surrounding motif, but lacks the aspartate and serine residues. Positions of some cysteine residues are also conserved in the pseudogene. This pseudogene lacks intronic sequences and should thus be classified as a processed pseudogene. EST and PCR analyses indicate that this pseudogene may be transcriptionally active, because mRNA was detected in many tissues including the prostate, testis, pituitary, and adrenal glands, as well as in tissues of the female genital organs. DISCUSSION: The mRNA sequence of the gene is, however, defective and is not predicted to code for a protein. Highly conserved sequences were found in the flanking region of the pseudogene, thus supporting the view that it evolved by retrotransposition. We also identified another serine protease fragment that has only the conserved histidine residue. The functional significance of the pseudogene and the other fragment is yet to be identified.

Amino Acid Sequence↗
PubMed2005

Distinctly different msp2 pseudogene repertoires in Anaplasma marginale strains that are capable of superinfection.

Lifelong persistent infection of cattle is a hallmark of the tick transmitted pathogen Anaplasma marginale. Antigenic variation of Major Surface Protein 2 (MSP2) plays an important role in evasion of the host immune response to allow persistence. Antigenic variation of MSP2 is achieved by gene conversion of pseudogenes into the single operon linked expression site and the diversity of variants is defined by the pseudogene repertoire. Once an animal is persistently infected with one strain of A. marginale, infection with a second strain (superinfection) is rare. However, we recently detected animals superinfected with different strains of A. marginale and hypothesized that the msp2 pseudogene repertoire would be distinct in these superinfecting strains, consistent with encoding different sets of surface variants. Five strains of A. marginale were selected in order to identify and compare msp2 pseudogene content; these included strains with similar and different msp1alpha genotypes, and genotypes that were representative of the strains that were found in the superinfected animals. Southern blot analysis of strains associated with superinfection revealed distinctly different msp2 banding patterns, in contrast to a pattern suggesting identical pseudogene content among related strains not associated with superinfection. Indeed, targeted sequence analysis of msp2 pseudogenes showed identical pseudogene repertoires in genotypically closely related strains and varying amounts of dissimilarity in the pseudogene repertoire in strains with distinctly different msp1alpha genotypes, but totally different msp2 pseudogene repertoires between the strains that were found in superinfected animals. This finding supports the hypothesis that the occurrence of superinfection reflects the differences in the msp2 repertoire and corresponding diversity of variants.

Amino Acid Sequence↗
PubMed2006

Frequent emergence and functional resurrection of processed pseudogenes in the human and mouse genomes.

Despite the wide distribution of processed pseudogenes in mammalian genomes, such as those of human and mouse, relatively little is known about their roles in genomic evolution. While gene duplications are recognized as one of the major driving forces in genome evolution, processed pseudogenes, which are retrotransposed copies of mRNAs, have been regarded as junk or selfish DNA for a long time. In order to elucidate the quantitative and qualitative contribution of processed pseudogenes to the mammalian genome evolution, we attempted to detect processed pseudogenes by extensively mapping the mRNAs to both the human and mouse genomes, and then we estimated the rate of their emergence. As a result, we revealed that the rate of pseudogene emergence was about 1-2% per gene per million years, which was as high as the rate (0.9%) of gene duplication in the human genome, although the rate of pseudogene emergence was found to drastically decrease in the hominid lineage. Furthermore, 1% of the processed pseudogenes seemed to be reinvigorated by post-retrotransposition transcription, many of them preserving the intact coding regions. Since the expression patterns of transcribed pseudogenes in various tissues were quite different between human and mouse, their emergence might have led to species-specific evolution. Our results indicate that the generation of processed pseudogenes was not wholly futile but instead has been an indispensable resource, driving dynamic evolution of the mammalian genomes.

Amino Acid Sequence↗
PubMed2002

A systematic investigation identifies a significant number of probable pseudogenes in the Escherichia coli genome.

Pseudogenes are open reading frames (ORFs) encoding dysfunctional proteins with high homology to known protein-coding genes. Although pseudogenes were reported to exist in the genomes of many eukaryotes and bacteria, no systematic search for pseudogenes in the Escherichia coli genome has been carried out. Genome comparisons of E. coli strains K-12 and O157 revealed that many protein-coding sequences have prematurely terminated orthologs encoding unstable proteins. To systematically screen for pseudogenes, we selected ORFs generated by premature termination of the orthologous protein-coding genes and subsequently excluded those possibly arising from sequence errors. Lastly we eliminated those with close homologs in this and other species, as these shortened ORFs may actually have functions. The process produced 95 and 101 pseudogene candidates in K-12 and O157, respectively. The assigned three-dimensional structures suggest that most of the encoded proteins cannot fold properly and thus are dysfunctional, indicating that they are probably pseudogenes. Therefore, the existence of a significant number of probable pseudogenes in E. coli is predicted, awaiting experimental verification. Most of them were found to be genes with paralogs or horizontally transferred genes or both. We suggest that pseudogenes constitute a small fraction of the genomes of free-living bacteria in general, reflecting the faster elimination than production of pseudogenes.

Amino Acid Sequence↗
PubMed2004

Improved techniques for the identification of pseudogenes.

MOTIVATION: Pseudogenes are the remnants of genomic sequences of genes which are no longer functional. They are frequent in most eukaryotic genomes, and an important resource for comparative genomics. However, pseudogenes are often mis-annotated as functional genes in sequence databases. Current methods for identifying pseudogenes include methods which rely on the presence of stop codons and frameshifts, as well as methods based on the ratio of non-silent to silent nucleotide substitution rates (dN/dS). A recent survey concluded that 50% of human pseudogenes have no detectable truncation in their pseudo-coding regions, indicating that the former methods lack sensitivity. The latter methods have been used to find sets of genes enriched for pseudogenes, but are not specific enough to accurately separate pseudogenes from expressed genes. RESULTS: We introduce a program called pseudogene inference from loss of constraint (PSILC) which incorporates novel methods for separating pseudogenes from functional genes. The methods calculate the log-odds score that evolution along the final branch of the gene tree to the query gene has been according to the following constraints: A neutral nucleotide model compared to a Pfam domain encoding model (PSILC(nuc/dom)); A protein coding model compared to a Pfam domain encoding model (PSILC(prot/dom)). Using the manual annotation of human chromosome 6, we show that both these methods result in a more accurate classification of pseudogenes than dN/dS when a Pfam domain alignment is available. AVAILABILITY: PSILC is available from http://www.sanger.ac.uk/Software/PSILC

Algorithms↗
PubMed2006

Systematic identification of pseudogenes through whole genome expression evidence profiling.

The identification of pseudogenes is an integral and significant part of the genome annotation because of their abundance and their impact on the experimental analysis of functional genes. Most of the computational annotation systems are not optimized for systematic pseudogene recognition, often annotating pseudogenes as functional genes, and users then propagate these errors to subsequent analyses and interpretations. In order to validate gene annotations and to identify pseudogenes that are potentially mis-annotated, we developed a novel approach based on whole genome profiling of existing transcript and protein sequences. This method has two important features: (i) equally detects both processed and non-processed pseudogenes and (ii) can identify transcribed pseudogenes. Applying this method to the human Ensembl gene predictions, we discovered that 2011 (9% of total) Ensembl genes in the categories of known and novel might be pseudogenes based on expression evidence. Of these, 1200 genes are found to have no existing evidence of transcription, and 811 genes are found with transcription evidence but contain significant translation disruption. Approximately 40% of the 2011 identified pseudogenes presented a multi-exon structure, representing non-processed pseudogenes. We have demonstrated the power of whole genome profiling of expression sequences to improve the accuracy of gene annotations.

Computational Biology↗
PubMed2004

Comprehensive analysis of pseudogenes in prokaryotes: widespread gene decay and failure of putative horizontally transferred genes.

BACKGROUND: Pseudogenes often manifest themselves as disabled copies of known genes. In prokaryotes, it was generally believed (with a few well-known exceptions) that they were rare. RESULTS: We have carried out a comprehensive analysis of the occurrence of pseudogenes in a diverse selection of 64 prokaryote genomes. Overall, we find a total of around 7,000 candidate pseudogenes. Moreover, in all the genomes surveyed, pseudogenes occur in at least 1 to 5% of all gene-like sequences, with some genomes having considerably higher occurrence. Although many large populations of pseudogenes arise from large, diverse protein families (for example, the ABC transporters), notable numbers of pseudogenes are associated with specific families that do not occur that widely. These include the cytochrome P450 and PPE families (PF00067 and PF00823) and others that have a direct role in DNA transposition. CONCLUSIONS: We find suggestive evidence that a large fraction of prokaryote pseudogenes arose from failed horizontal transfer events. In particular, we find that pseudogenes are more than twice as likely as genes to have anomalous codon usage associated with horizontal transfer. Moreover, we found a significant difference in the number of horizontally transferred pseudogenes in pathogenic and non-pathogenic strains of Escherichia coli.

Escherichia coli K12↗
PubMedDate not supplied

[Pseudogenes: structure conservation, expression, and functions].

Pseudogenes have been defined as nonfunctional sequences of genomic DNA (junk DNA) originally derived from functional genes. It is therefore assumed that pseudogenes are not subject to natural selection and consequently pseudogene mutations are selectively neutral and have equal probability to become fixed in the population. We describe some unexpected features of pseudogenes in diverse organisms that are inconsistent with this widely accepted point of view. Pseudogenes are often evolutionary conserved and transcriptionally active. Moreover, pseudogenes that have been suitably investigated often exhibit functional roles, such as gene regulation, generation of genetic diversity, and other features that are expected in genes or DNA sequences that have functional roles. A review of the evidence leads to the conclusion that pseudogenes are important components of genomes, representing a repertoire of sequences available for functional evolution and subject to non-neutral evolutionary changes. Pseudogenes might be considered as potogenes, i.e. DNA sequences with a potentiality for becoming new genes or acquire new functions. Furthermore we conjecture that some pseudogenes along with their parental sequences may constitute sets of indivisible functionally interacting entities (intergenic complexes or "intergenes"), in which all the component elements are required in order to fulfill a collective functional role.

Animals↗
PubMed1984

Pseudogenes for human U2 small nuclear RNA do not have a fixed site of 3' truncation.

We present the sequences of five additional human U2 pseudogenes which are very similar to the U2.13 pseudogene reported previously [Van Arsdell et al. (1981) Cell 26, 11-17]. All six U2 pseudogenes preserve the 5' end of the mature U2 snRNA sequence, and all six are flanked by nearly perfect direct repeats that differ in sequence and range in length from 16 to 21 base pairs. The 3' ends of the six U2 pseudogenes are truncated at five different sites between position 33 and 82, and in two cases the 3' end of the pseudogene overlaps the downstream direct repeat by 5 or 6 base pairs. The structure of these six U2 pseudogenes contrasts with that of four human U3 pseudogenes [Bernstein et al. (1983) Cell 32, 461-472] all of which are identically truncated at position 69 or 70, and appear to be derived from a self-primed 74 base reverse transcript of U3 snRNA. Comparison of the U2 and U3 pseudogenes suggests a model for their generation in which the 3' end of the pseudogene is always truncated relative to the initial cDNA template.

Bacteriophage lambda↗
PubMed1993

Isolation and characterization of a human pseudogene for the regulatory subunit RI alpha of cAMP-dependent protein kinases and its sublocalization on chromosome 1.

Using a human cDNA (complementary DNA) encoding the regulatory subunit RI alpha of cAMP-dependent protein kinases (PKA) as a probe, a pseudogene for this PKA isoform was isolated from a human genomic library. The human RI alpha pseudogene was 89% similar to the open reading frame of the expressed human RI alpha at the nucleotide level. Several stop codons were found, indicating that the pseudogene does not encode a functional protein. The pseudogene also contained several frameshift mutations, small deletions, and insertions. No introns were found in the region corresponding to the open reading frame of the expressed RI alpha cDNA. Specific oligonucleotides for the RI alpha gene and pseudogene were constructed and used as primers in polymerase chain reaction (PCR) to amplify human DNA from healthy blood donors. Probing of the PCR products using oligonucleotides specific for the RI alpha gene and RI alpha pseudogene, respectively, showed the presence of both genes in the human genome. When DNA extracted from various somatic cell hybrids was amplified, it was shown that the RI alpha gene was located on human chromosome 17, whereas the RI alpha pseudogene was located in the p21-p31 region on chromosome 1. This is the first report describing a pseudogene for a subunit of cAMP-dependent protein kinases from any species.

Amino Acid Sequence↗
PubMed1994

Molecular analysis of functional and nonfunctional genes for human ferrochelatase: isolation and characterization of a FECH pseudogene and its sublocalization on chromosome 3.

A pseudogene related to the functional gene (FECH) for the heme biosynthetic enzyme ferrochelatase (ferroheme-protolyase; EC 4.99.1.1.) was isolated from a human genomic library using a ferrochelatase cDNA hybridization probe. The pseudogene shows > 80% overall nucleotide sequence identity to the functional gene (including the 3' untranslated region and polyadenylation signals) but contains no intronic sequences in the region corresponding to the open reading frame of expressed ferrochelatase. Furthermore, the pseudogene sequence contains small deletions and insertions creating frameshifts and numerous termination codons, indicating that it does not encode a functional polypeptide. Northern blot analysis using pseudogene-specific probes failed to demonstrate transcripts in samples of human erythroid cell RNA in which ferrochelatase mRNA was readily detected. Southern blot experiments using restriction endonuclease-digested human genomic DNA probed either with ferrochelatase-specific cDNA fragments or pseudogene-specific genomic sequences confirmed the presence of distinct loci for the expressed and nonfunctional genes, respectively. Localization of the human ferrochelatase pseudogene to 3p22-p23 was determined by fluorescent metaphase chromosomal hybridization in situ using three genomic clones in lambda EMBL3 spanning a contiguous region of approximately 30 kb. This newly identified locus, distinct from the expressed FECH gene, on 18q22, is characteristic of a processed human pseudogene. The existence of the ferrochelatase pseudogene has practical implications for the molecular analysis of mutations responsible for erythropoietic protoporphyria in man.

Amino Acid Sequence↗
PubMed1991

Two closely related kappa variable region pseudogenes pose an evolutionary paradox.

Two pseudogenes belonging to the Igk-V1 variable region group have been isolated from BALB/c mice. The genes share greater than 96.5% identity of nucleotide sequence in a 1800 base pair (bp) region surrounding the coding region, but deletions of 221 bp and 84 bp have removed essential sequences from the two genes. As the deletions are different in the two pseudogenes, they must have occurred independently in each gene during or subsequent to the duplication event which gave rise to the genes from a common ancestral gene. Polymerase chain reaction analysis was used to identify the pseudogenes in inbred strains of mice. BALB/c (Igkc) and AKR (Igka), prototype strains representative of the predominant kappa haplotypes, possess both pseudogenes but no intact copy. Only one of the pseudogenes was present in SJL (Igka). Strains C58, c.C58 (Igkd) and NZB (Igkb) possessed an intact version of the gene. This distribution of haplotypes is consistent with a close linkage of the pseudogenes with other Igk-V1 genes on chromosome 6. The translated amino acid sequence of the pseudogenes indicates that prior to their acquiring deletions they encoded typical Igk-V1 variable regions except for an unusual FR2 region, in which the conserved proline at position 44 is replaced by leucine and the normally hydrophobic position 36 was occupied by histidine. Possible mechanisms to explain the occurrence of deletions in both of the pseudogenes in the recent evolution of BALB/c are discussed. One explanation would be that the two genes were already nonfunctional at the time of the duplication so that the subsequent deletions represent neutral events which became fixed in the inbred strains by a process of genetic drift. Alternatively, if the genes were functional at the time of duplication, their rapid loss due to deletion events suggests that negative selection may have acted to eliminate the genes from the V-region repertoire.

Alleles↗
PubMed2004

A new role for expressed pseudogenes as ncRNA: regulation of mRNA stability of its homologous coding gene.

We have earlier generated a mutant mouse in a course of making a transgenic line that exhibited interesting heterozygote phenotypes, which exhibited failure to thrive, severe bone deformities, and polycystic kidneys. This mutant mouse provided a clue to uncover a unique role of expressed pseudogenes. In this mutant the transgene was integrated into the vicinity of the expressing pseudogene of Makorin1 called Makorin1-p1. This insertion reduced transcription of the Makorin1-p1, resulting in destabilization of the Makorin1 mRNA in trans via a cis-acting RNA decay element within the 5' region of Makorin1 that is homologous between Makorin1 and Makorin1-p1. These findings demonstrate a novel and specific regulatory role of an expressed pseudogene as well as functional significance for noncoding RNAs. Next, we developed an original algorithm to determine how many pseudogenes are expressed. Based on our examination 2-3% of human processed pseudogenes are expressed using the most strict criteria. Interestingly, the mouse has a much smaller proportion of expressed pseudogenes (0.5-1%). Pseudogenes are functionally less constrained, and have accumulated more mutations than translated genes. If they have some functions in gene regulation, this property would allow more rapid functional diversification than protein-coding genes. In addition, some genetic phenomena that exhibit incomplete penetrance might be attributed to "mutation" or "variation" of pseudogenes.

Animals↗
PubMed2003

The human genome has 49 cytochrome c pseudogenes, including a relic of a primordial gene that still functions in mouse.

Using a computational approach, we have identified 49 cytochrome c (cyc) pseudogenes in the human genome. Analysis of these provides a detailed description of the molecular evolution of the cyc gene. Almost all of the pseudogenes are full-length, and we have concluded that they mostly originated from independent retrotransposition events (i.e. they are processed). Based on phylogenetic analysis and detailed sequence comparison, we have further divided these pseudogenes into two groups. The first, consisting of four young pseudogenes that were dated to be between 27 and 34 Myr old, originated from a gene almost identical to the modern human cyc gene. The second group of pseudogenes is much older and appears to have descended from ancient genes similar to modern rodent cyc genes. Thus, our results support the observation that accelerated evolution in cyc sequence had occurred in the primate lineage. The oldest pseudogene in the second group, dated to be over 80 Myr old, resembles the testis-specific cyc gene in modern rodents. It is likely that the mammalian ancestor had both the somatic and the testis-specific cyc genes. While the testis-specific gene is still functional in modern rodents, the human has lost it, retaining only a pseudogene in its place. Thus, our study may have identified a pseudogene that is a dead relic of a gene that has completely died off in the human lineage.

Amino Acid Sequence↗