Gene redundancy

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Gene redundancy is the existence of multiple genes in the genome of an organism that perform the same function. Gene redundancy can result from gene duplication. [1] Such duplication events are responsible for many sets of paralogous genes. [1] When an individual gene in such a set is disrupted by mutation or targeted knockout, there can be little effect on phenotype as a result of gene redundancy, whereas the effect is large for the knockout of a gene with only one copy. [2] Gene knockout is a method utilized in some studies aiming to characterize the maintenance and fitness effects functional overlap. [3]

Contents

Classical models of maintenance propose that duplicated genes may be conserved to various extents in genomes due to their ability to compensate for deleterious loss of function mutations. [4] [5] These classical models do not take into account the potential impact of positive selection. Beyond these classical models, researchers continue to explore the mechanisms by which redundant genes are maintained and evolve. [6] [7] [8] Gene redundancy has long been appreciated as a source of novel gene origination; [8] that is, new genes may arise when selective pressure exists on the duplicate, while the original gene is maintained to perform the original function, as proposed by newer models [4] .

Figure 1. Common mechanisms of gene duplication. Gene Duplication.jpg
Figure 1. Common mechanisms of gene duplication.

Origin and Evolution of Redundant Genes

Gene redundancy most often results from Gene duplication. [9] Three of the more common mechanisms of gene duplication are retroposition, unequal crossing over, and non-homologous segmental duplication. Retroposition is when the mRNA transcript of a gene is reverse transcribed back into DNA and inserted into the genome at a different location. During unequal crossing over, homologous chromosomes exchange uneven portions of their DNA. This can lead to the transfer of one chromosome's gene to the other chromosome, leaving two of the same gene on one chromosome, and no copies of the gene on the other chromosome. Non-homologous duplications result from replication errors that shift the gene of interest into a new position. A tandem duplication then occurs, creating a chromosome with two copies of the same gene. Figure 1 provides a visualization of these three mechanisms. [10] When a gene is duplicated within a genome, the two copies are initially functionally redundant. These redundant genes are considered paralogs as they accumulate changes over time, until they functionally diverge. [11]

Much research is centered around the question of how redundant genes persist. [12] Three models have arisen to attempt to explain preservation of redundant genes: adaptive radiation, divergence, and escape from adaptive conflict. Notably, retainment following a duplication event is influenced by type of duplication event and type of gene class. That is, some gene classes are better suited for redundancy following a small scale duplication or whole genome duplication event. [13] Redundant genes are more likely to survive when they are involved in complex pathways and are the product of whole genome duplication or multifamily duplication. [13]

The currently accepted outcomes for single gene duplicates include: gene loss (non-functionalization), functional divergence, and conservation for increased genetic robustness. [11] Otherwise, multigene families may undergo concerted evolution, or birth and death evolution. [11] Concerted evolution is the idea that genes in a group, such as a gene family, evolve in parallel. [11] The birth death evolution concept is that the gene family undergoes strong purifying selection. [11]

Functional Divergence

As the genome replicates over many generations, the redundant gene's function will most likely evolve due to Genetic drift. Genetic drift influences genetic redundancy by either eliminating variants or fixing variants in the population. [12] In the event that genetic drift maintains the variants, the gene may accumulate mutations that change the overall function. [14] However, many redundant genes may diverge but retain original function by mechanisms such as subfunctionalization, which preserves original gene function albeit by complementary action of the duplicates. [13] [12] The three mechanisms of functional divergence in genes are nonfunctionalization (or gene loss), neofunctionalization and subfunctionalization. [11]

During nonfunctionalization, or degeneration/gene loss, one copy of the duplicated gene acquires mutations that render it inactive or silent. Non-functionalization is often the result of single gene duplications. [11] At this time, the gene has no function and is called a pseudogene. Pseudogenes can be lost over time due to genetic mutations. Neofunctionalization occurs when one copy of the gene accumulates mutations that give the gene a new, beneficial function that is different than the original function. Subfunctionalization occurs when both copies of the redundant gene acquire mutations. Each copy becomes only partially active; two of these partial copies then act as one normal copy of the original gene. Figure 2 to the right provides a visualization of this concept.

Transposable Elements

Transposable elements play various roles in functional differentiation. By enacting recombination, transposable elements can move redundant sequences in the genome. [15] This change in sequence structure and location is a source of functional divergence. [15] Transposable elements potentially impact gene expression, given that they contain a sizeable amount of micro-RNAs. [15]

Gene Maintenance Hypotheses

The evolution and origin of redundant genes remain unknown, largely because evolution happens over such a long period of time. Theoretically, a gene can not be maintained without mutation unless it has a selective pressure acting on it. Gene redundancy, therefore, would allow both copies of the gene to accumulate mutations as long as the other was still able to perform its function. This means that all redundant genes should theoretically become a pseudogene and eventually be lost. Scientists have devised two hypotheses as to why redundant genes can remain in the genome: the backup hypothesis and the piggyback hypothesis. [16]

The backup hypothesis proposes that redundant genes remain in the genome as a sort of "back-up plan". If the original gene loses its function, the redundant gene is there to take over and keep the cell alive. The piggyback hypothesis states that two paralogs in the genome have some kind of non-overlapping function as well as the redundant function. In this case, the redundant part of the gene remains in the genome due to the proximity to the area that codes for the unique function. [17] The reason redundant genes remain in the genome is an ongoing question and gene redundancy is being studied by researchers everywhere. There are many hypotheses in addition to the backup and piggyback models. For example, at the University of Michigan, a study provides the theory that redundant genes are maintained in the genome by reduced expression.

Research

Gene Families and Phylogeny

Researchers often use the history of redundant genes in the form of gene families to learn about the phylogeny of a species. It takes time for redundant genes to undergo functional diversification; the degree of diversification between orthologs tells us how closely related the two genomes are. Gene duplication events can also be detected by looking at increases in gene duplicates.

A good example of using gene redundancy in evolutionary studies is the Evolution of the KCS gene family in plants. This paper studies how one KCS gene evolved into an entire gene family via duplication events. The number of redundant genes in the species allows researchers to determine when duplication events took place and how closely related species are.

Locating and Characterizing Redundant Genes

Currently, there are three ways to detect paralogs in a known genomic sequence: simple homology (FASTA), gene family evolution (TreeFam) and orthology (eggNOG v3). Researchers often construct phylogenies and utilize microarrays to compare the structures of genomes to identify redundancy. [18] Methods like creating syntenic alignments and analysis of orthologous regions are used to compare multiple genomes. Single genomes can be scanned for redundant genes using exhaustive pairwise comparisons. [18] Before performing more laborious analyses of redundant genes, researchers typically test for functionality by comparing open reading frame length and the rates between silent and non-silent mutations. [18] Since the Human Genome Project's completion, researchers are able to annotate the human genome much more easily. Using online databases like the Genome Browser at UCSC, researchers can look for homology in the sequence of their gene of interest.

Breast Cancer Disposition Genes

The mode of duplication by which redundancy occurs has been found to impact the classifications in breast cancer disposition genes. [19] Gross duplications complicate clinical interpretation because it is difficult to discern if they occur in tandem. Recent methods, like DNA breakpoint assay, have been used to determine tandem status. [19] In turn, these tandem gross duplications can be more accurately screened for pathogenic status. [19] This research has important implications for evaluating risk of breast cancer. [19]

Pathogen Resistance in Triticeae grasses

Researchers have also identified redundant genes that confer selective advantage on the organismal level. The partial ARM1 gene, a redundant gene resulting from a partial duplication, has been found to confer resistance to Blumeria graminis , a mildew fungus. [20] This gene exists in members of the Triticeae tribe, including wheat, rye, and barley. [20]

Human Redundant Genes

Olfactory Receptors

The Human Olfactory Receptor (OR) gene family contains 339 intact genes and 297 pseudogenes. These genes are found in different locations throughout the genome, but only about 13% are on different chromosomes or on distantly spaced loci. 172 subfamilies of OR genes have been found in humans, each at its own loci. Because the genes in each of these subfamilies are structurally and functionally similar, and in close proximity to each other, it is hypothesized that each evolved from single genes undergoing duplication events. The high number of subfamilies in humans explains why we are able to recognize so many odors.

Human OR genes have homologues in other mammals, such as mice, that demonstrate the evolution of Olfactory Receptor genes. One particular family that is involved in the initial event of odor perception has been found to be highly conserved throughout all of vertebrate evolution. [21]

Disease

Duplication events and redundant genes have often been thought to have a role in some human diseases. Large scale whole genome duplication events that occurred early in vertebrate evolution may be the reason that human monogenic disease genes often contain a high number of redundant genes. Chen et al. hypothesizes that the functionally redundant paralogs in human monogenic disease genes mask the effects of dominant deleterious mutations, thereby maintaining the disease gene in the human genome. [22]

Whole genome duplications may be a leading cause of retention of some tumor causing genes in the human genome. [23] For example, Strout et al. [24] have shown that tandem duplication events, likely via homologous recombination, are linked to acute myeloid leukemia. The partial duplication of the ALL1 (MLL) gene is a genetic defect has been found in patients with acute myeloid leukemia.

Related Research Articles

An intron is any nucleotide sequence within a gene that is not expressed or operative in the final RNA product. The word intron is derived from the term intragenic region, i.e., a region inside a gene. The term intron refers to both the DNA sequence within a gene and the corresponding RNA sequence in RNA transcripts. The non-intron sequences that become joined by this RNA processing to form the mature RNA are called exons.

Microevolution is the change in allele frequencies that occurs over time within a population. This change is due to four different processes: mutation, selection, gene flow and genetic drift. This change happens over a relatively short amount of time compared to the changes termed macroevolution.

<span class="mw-page-title-main">Mutation</span> Alteration in the nucleotide sequence of a genome

In biology, a mutation is an alteration in the nucleic acid sequence of the genome of an organism, virus, or extrachromosomal DNA. Viral genomes contain either DNA or RNA. Mutations result from errors during DNA or viral replication, mitosis, or meiosis or other types of damage to DNA, which then may undergo error-prone repair, cause an error during other forms of repair, or cause an error during replication. Mutations may also result from insertion or deletion of segments of DNA due to mobile genetic elements.

<span class="mw-page-title-main">Human genome</span> Complete set of nucleic acid sequences for humans

The human genome is a complete set of nucleic acid sequences for humans, encoded as DNA within the 23 chromosome pairs in cell nuclei and in a small DNA molecule found within individual mitochondria. These are usually treated separately as the nuclear genome and the mitochondrial genome. Human genomes include both protein-coding DNA sequences and various types of DNA that does not encode proteins. The latter is a diverse category that includes DNA coding for non-translated RNA, such as that for ribosomal RNA, transfer RNA, ribozymes, small nuclear RNAs, and several types of regulatory RNAs. It also includes promoters and their associated gene-regulatory elements, DNA playing structural and replicatory roles, such as scaffolding regions, telomeres, centromeres, and origins of replication, plus large numbers of transposable elements, inserted viral DNA, non-functional pseudogenes and simple, highly repetitive sequences. Introns make up a large percentage of non-coding DNA. Some of this non-coding DNA is non-functional junk DNA, such as pseudogenes, but there is no firm consensus on the total amount of junk DNA.

Molecular evolution is the process of change in the sequence composition of cellular molecules such as DNA, RNA, and proteins across generations. The field of molecular evolution uses principles of evolutionary biology and population genetics to explain patterns in these changes. Major topics in molecular evolution concern the rates and impacts of single nucleotide changes, neutral evolution vs. natural selection, origins of new genes, the genetic nature of complex traits, the genetic basis of speciation, the evolution of development, and ways that evolutionary forces influence genomic and phenotypic changes.

<span class="mw-page-title-main">Pseudogene</span> Functionless relative of a gene

Pseudogenes are nonfunctional segments of DNA that resemble functional genes. Most arise as superfluous copies of functional genes, either directly by gene duplication or indirectly by reverse transcription of an mRNA transcript. Pseudogenes are usually identified when genome sequence analysis finds gene-like sequences that lack regulatory sequences needed for transcription or translation, or whose coding sequences are obviously defective due to frameshifts or premature stop codons. Pseudogenes are a type of junk DNA.

Gene duplication is a major mechanism through which new genetic material is generated during molecular evolution. It can be defined as any duplication of a region of DNA that contains a gene. Gene duplications can arise as products of several types of errors in DNA replication and repair machinery as well as through fortuitous capture by selfish genetic elements. Common sources of gene duplications include ectopic recombination, retrotransposition event, aneuploidy, polyploidy, and replication slippage.

<span class="mw-page-title-main">Gene family</span> Set of several similar genes

A gene family is a set of several similar genes, formed by duplication of a single original gene, and generally with similar biochemical functions. One such family are the genes for human hemoglobin subunits; the ten genes are in two clusters on different chromosomes, called the α-globin and β-globin loci. These two gene clusters are thought to have arisen as a result of a precursor gene being duplicated approximately 500 million years ago.

<span class="mw-page-title-main">Sequence homology</span> Shared ancestry between DNA, RNA or protein sequences

Sequence homology is the biological homology between DNA, RNA, or protein sequences, defined in terms of shared ancestry in the evolutionary history of life. Two segments of DNA can have shared ancestry because of three phenomena: either a speciation event (orthologs), or a duplication event (paralogs), or else a horizontal gene transfer event (xenologs).

<span class="mw-page-title-main">Copy number variation</span> Repeated DNA variation between individuals

Copy number variation (CNV) is a phenomenon in which sections of the genome are repeated and the number of repeats in the genome varies between individuals. Copy number variation is a type of structural variation: specifically, it is a type of duplication or deletion event that affects a considerable number of base pairs. Approximately two-thirds of the entire human genome may be composed of repeats and 4.8–9.5% of the human genome can be classified as copy number variations. In mammals, copy number variations play an important role in generating necessary variation in the population as well as disease phenotype.

<span class="mw-page-title-main">Gene</span> Sequence of DNA or RNA that codes for an RNA or protein product

In biology, the word gene has two meanings. The Mendelian gene is a basic unit of heredity. The molecular gene is a sequence of nucleotides in DNA, that is transcribed to produce a functional RNA. There are two types of molecular genes: protein-coding genes and non-coding genes.

<span class="mw-page-title-main">Gene cluster</span>

A gene family is a set of homologous genes within one organism. A gene cluster is a group of two or more genes found within an organism's DNA that encode similar polypeptides, or proteins, which collectively share a generalized function and are often located within a few thousand base pairs of each other. The size of gene clusters can vary significantly, from a few genes to several hundred genes. Portions of the DNA sequence of each gene within a gene cluster are found to be identical; however, the resulting protein of each gene is distinctive from the resulting protein of another gene within the cluster. Genes found in a gene cluster may be observed near one another on the same chromosome or on different, but homologous chromosomes. An example of a gene cluster is the Hox gene, which is made up of eight genes and is part of the Homeobox gene family.

<span class="mw-page-title-main">Cat genetics</span> Study of inheritance in domestic cats

Cat genetics describes the study of inheritance as it occurs in domestic cats. In feline husbandry it can predict established traits (phenotypes) of the offspring of particular crosses. In medical genetics, cat models are occasionally used to discover the function of homologous human disease genes.

Functional divergence is the process by which genes, after gene duplication, shift in function from an ancestral function. Functional divergence can result in either subfunctionalization, where a paralog specializes one of several ancestral functions, or neofunctionalization, where a totally new functional capability evolves. It is thought that this process of gene duplication and functional divergence is a major originator of molecular novelty and has produced the many large protein families that exist today.

<span class="mw-page-title-main">Subfunctionalization</span>

Subfunctionalization was proposed by Stoltzfus (1999) and Force et al. (1999) as one of the possible outcomes of functional divergence that occurs after a gene duplication event, in which pairs of genes that originate from duplication, or paralogs, take on separate functions. Subfunctionalization is a neutral mutation process of constructive neutral evolution; meaning that no new adaptations are formed. During the process of gene duplication paralogs simply undergo a division of labor by retaining different parts (subfunctions) of their original ancestral function. This partitioning event occurs because of segmental gene silencing leading to the formation of paralogs that are no longer duplicates, because each gene only retains a single function. It is important to note that the ancestral gene was capable of performing both functions and the descendant duplicate genes can now only perform one of the original ancestral functions.

Evolution by gene duplication is an event by which a gene or part of a gene can have two identical copies that can not be distinguished from each other. This phenomenon is understood to be an important source of novelty in evolution, providing for an expanded repertoire of molecular activities. The underlying mutational event of duplication may be a conventional gene duplication mutation within a chromosome, or a larger-scale event involving whole chromosomes (aneuploidy) or whole genomes (polyploidy). A classic view, owing to Susumu Ohno, which is known as Ohno model, he explains how duplication creates redundancy, the redundant copy accumulates beneficial mutations which provides fuel for innovation. Knowledge of evolution by gene duplication has advanced more rapidly in the past 15 years due to new genomic data, more powerful computational methods of comparative inference, and new evolutionary models.

<span class="mw-page-title-main">Genome evolution</span> Process by which a genome changes in structure or size over time

Genome evolution is the process by which a genome changes in structure (sequence) or size over time. The study of genome evolution involves multiple fields such as structural analysis of the genome, the study of genomic parasites, gene and ancient genome duplications, polyploidy, and comparative genomics. Genome evolution is a constantly changing and evolving field due to the steadily growing number of sequenced genomes, both prokaryotic and eukaryotic, available to the scientific community and the public at large.

<span class="mw-page-title-main">Unequal crossing over</span> Chromosomal crossover resulting in gene duplication or deletion

Unequal crossing over is a type of gene duplication or deletion event that deletes a sequence in one strand and replaces it with a duplication from its sister chromatid in mitosis or from its homologous chromosome during meiosis. It is a type of chromosomal crossover between homologous sequences that are not paired precisely. Normally genes are responsible for occurrence of crossing over. It exchanges sequences of different links between chromosomes. Along with gene conversion, it is believed to be the main driver for the generation of gene duplications and is a source of mutation in the genome.

<span class="mw-page-title-main">Neofunctionalization</span>

Neofunctionalization, one of the possible outcomes of functional divergence, occurs when one gene copy, or paralog, takes on a totally new function after a gene duplication event. Neofunctionalization is an adaptive mutation process; meaning one of the gene copies must mutate to develop a function that was not present in the ancestral gene. In other words, one of the duplicates retains its original function, while the other accumulates molecular changes such that, in time, it can perform a different task.

Diploidization is the process of converting a polyploid genome back into a diploid one. Polyploidy is a product of whole genome duplication (WGD) and is followed by diploidization as a result of genome shock. The plant kingdom has undergone multiple events of polyploidization followed by diploidization in both ancient and recent lineages. It has also been hypothesized that vertebrate genomes have gone through two rounds of paleopolyploidy. The mechanisms of diploidization are poorly understood but patterns of chromosomal loss and evolution of novel genes are observed in the process.

References

  1. 1 2 Conrad, Bernard; Antonarakis, Stylianos E. (September 2007). "Gene Duplication: A Drive for Phenotypic Diversity and Cause of Human Disease". Annual Review of Genomics and Human Genetics. 8 (1): 17–35. doi:10.1146/annurev.genom.8.021307.110233. ISSN   1527-8204. PMID   17386002.
  2. ↑ Pérez-Pérez JM, Candela H, Micol JL (August 2009). "Understanding synergy in genetic interactions". Trends Genet. 25 (8): 368–76. doi:10.1016/j.tig.2009.06.004. PMID   19665253.
  3. ↑ Pérez-Pérez, José Manuel; Candela, Héctor; Micol, José Luis (2009-08-01). "Understanding synergy in genetic interactions". Trends in Genetics. 25 (8): 368–376. doi:10.1016/j.tig.2009.06.004. ISSN   0168-9525. PMID   19665253.
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  5. ↑ Martienssen, Rob; Irish, Vivian (1999-11-01). "Copying out our ABCs: the role of gene redundancy in interpreting genetic hierarchies". Trends in Genetics. 15 (11): 435–437. doi:10.1016/S0168-9525(99)01833-8. ISSN   0168-9525. PMID   10529802.
  6. ↑ Conrad, Bernard; Antonarakis, Stylianos E. (September 2007). "Gene Duplication: A Drive for Phenotypic Diversity and Cause of Human Disease". Annual Review of Genomics and Human Genetics. 8 (1): 17–35. doi:10.1146/annurev.genom.8.021307.110233. ISSN   1527-8204. PMID   17386002.
  7. ↑ Force A et al. 1999. Preservation of duplicate genes by complementary, degenerative mutations. Genetics. 151:1531–1545.
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  9. ↑ Wagner, Andreas (1996-06-01). "Genetic redundancy caused by gene duplications and its evolution in networks of transcriptional regulators". Biological Cybernetics. 74 (6): 557–567. doi:10.1007/BF00209427. ISSN   1432-0770. PMID   8672563. S2CID   8616418.
  10. ↑ Hurles, Matthew (2004-07-13). "Gene Duplication: The Genomic Trade in Spare Parts". PLOS Biology. 2 (7): e206. doi: 10.1371/journal.pbio.0020206 . ISSN   1545-7885. PMC   449868 . PMID   15252449.
  11. 1 2 3 4 5 6 7 Conrad, Bernard; Antonarakis, Stylianos E. (September 2007). "Gene Duplication: A Drive for Phenotypic Diversity and Cause of Human Disease". Annual Review of Genomics and Human Genetics. 8 (1): 17–35. doi:10.1146/annurev.genom.8.021307.110233. ISSN   1527-8204. PMID   17386002.
  12. 1 2 3 Long M, Vankuren NW, Chen S, Vibranovski MD. 2013. New gene evolution: Little did we know. Annu. Rev. Genet. 47:307–333. doi : 10.1146/annurev-genet-111212-133301
  13. 1 2 3 Conant, G. C.; Wolfe, K. H. (2008). "Turning a hobby into a job: How duplicated genes find new functions". Nature Reviews Genetics. 9 (12): 938–950. doi:10.1038/nrg2482. PMID   19015656. S2CID   1240225.
  14. ↑ Force A et al. 1999. Preservation of duplicate genes by complementary, degenerative mutations. Genetics. 151:1531–1545.
  15. 1 2 3 Platt, Roy N.; Vandewege, Michael W.; Ray, David A. (March 2018). "Mammalian transposable elements and their impacts on genome evolution". Chromosome Research. 26 (1–2): 25–43. doi: 10.1007/s10577-017-9570-z . ISSN   0967-3849. PMC   5857283 . PMID   29392473.
  16. ↑ Zhang, Jianzhi (2012). "Genetic Redundancies and Their Evolutionary Maintenance". Evolutionary Systems Biology. Advances in Experimental Medicine and Biology. Vol. 751. pp. 279–300. doi:10.1007/978-1-4614-3567-9_13. ISBN   978-1-4614-3566-2. PMID   22821463.{{cite book}}: |journal= ignored (help)
  17. ↑ Qian, Wenfeng; Liao, Ben-Yang; Chang, Andrew Y.-F.; Zhang, Jianzhi (2010-10-01). "Maintenance of duplicate genes and their functional redundancy by reduced expression". Trends in Genetics. 26 (10): 425–430. doi:10.1016/j.tig.2010.07.002. ISSN   0168-9525. PMC   2942974 . PMID   20708291.
  18. 1 2 3 Long M, Vankuren NW, Chen S, Vibranovski MD. 2013. New gene evolution: Little did we know. Annu. Rev. Genet. 47:307–333. doi : 10.1146/annurev-genet-111212-133301
  19. 1 2 3 4 Richardson, Marcy E.; Chong, Hansook; Mu, Wenbo; Conner, Blair R.; Hsuan, Vickie; Willett, Sara; Lam, Stephanie; Tsai, Pei; Pesaran, Tina; Chamberlin, Adam C.; Park, Min-Sun (2018-07-28). "DNA breakpoint assay reveals a majority of gross duplications occur in tandem reducing VUS classifications in breast cancer predisposition genes". Genetics in Medicine. 21 (3): 683–693. doi: 10.1038/s41436-018-0092-7 . ISSN   1098-3600. PMC   6752314 . PMID   30054569.
  20. 1 2 Rajaraman, Jeyaraman; Douchkov, Dimitar; Lück, Stefanie; Hensel, Götz; Nowara, Daniela; Pogoda, Maria; Rutten, Twan; Meitzel, Tobias; Brassac, Jonathan; Höfle, Caroline; Hückelhoven, Ralph (2018-08-15). "Evolutionarily conserved partial gene duplication in the Triticeae tribe of grasses confers pathogen resistance". Genome Biology. 19 (1): 116. doi: 10.1186/s13059-018-1472-7 . ISSN   1474-760X. PMC   6092874 . PMID   30111359.
  21. ↑ Malnic, Bettina; Godfrey, Paul A.; Buck, Linda B. (2004-02-24). "The human olfactory receptor gene family". Proceedings of the National Academy of Sciences of the United States of America. 101 (8): 2584–2589. Bibcode:2004PNAS..101.2584M. doi: 10.1073/pnas.0307882100 . ISSN   0027-8424. PMC   356993 . PMID   14983052.
  22. ↑ Chen, Wei-Hua; Zhao, Xing-Ming; van Noort, Vera; Bork, Peer (2013-05-01). "Human Monogenic Disease Genes Have Frequently Functionally Redundant Paralogs". PLOS Computational Biology. 9 (5): e1003073. Bibcode:2013PLSCB...9E3073C. doi: 10.1371/journal.pcbi.1003073 . ISSN   1553-734X. PMC   3656685 . PMID   23696728.
  23. ↑ Malaguti, Giulia; Singh, Param Priya; Isambert, Hervé (2014-05-01). "On the retention of gene duplicates prone to dominant deleterious mutations". Theoretical Population Biology. 93: 38–51. doi:10.1016/j.tpb.2014.01.004. ISSN   1096-0325. PMID   24530892.
  24. ↑ Strout, Matthew P.; Marcucci, Guido; Bloomfield, Clara D.; Caligiuri, Michael A. (1998-03-03). "The partial tandem duplication of ALL1 (MLL) is consistently generated by Alu-mediated homologous recombination in acute myeloid leukemia". Proceedings of the National Academy of Sciences of the United States of America. 95 (5): 2390–2395. Bibcode:1998PNAS...95.2390S. doi: 10.1073/pnas.95.5.2390 . ISSN   0027-8424. PMC   19353 . PMID   9482895.

Further reading

  1. ↑ Guo, Hai-Song; Zhang, Yan-Mei; Sun, Xiao-Qin; Li, Mi-Mi; Hang, Yue-Yu; Xue, Jia-Yu (2015-11-12). "Evolution of the KCS gene family in plants: the history of gene duplication, sub/neofunctionalization and redundancy". Molecular Genetics and Genomics. 291 (2): 739–752. doi:10.1007/s00438-015-1142-3. ISSN   1617-4615. PMID   26563433. S2CID   18320216.
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