scholarly journals Gene Duplication, Gene Conversion and the Evolution of the Y Chromosome

Genetics ◽  
2010 ◽  
Vol 186 (1) ◽  
pp. 277-286 ◽  
Author(s):  
Tim Connallon ◽  
Andrew G. Clark
Genetics ◽  
2021 ◽  
Author(s):  
Takahiro Sakamoto ◽  
Hideki Innan

Abstract Muller’s ratchet is a process in which deleterious mutations are fixed irreversibly in the absence of recombination. The degeneration of the Y chromosome, and the gradual loss of its genes, can be explained by Muller’s ratchet. However, most theories consider single-copy genes, and may not be applicable to Y chromosomes, which have a number of duplicated genes in many species, which are probably undergoing concerted evolution by gene conversion. We developed a model of Muller’s ratchet to explore the evolution of the Y chromosome. The model assumes a non-recombining chromosome with both single-copy and duplicated genes. We used analytical and simulation approaches to obtain the rate of gene loss in this model, with special attention to the role of gene conversion. Homogenization by gene conversion makes both duplicated copies either mutated or intact. The former promotes the ratchet, and the latter retards, and we ask which of these counteracting forces dominates under which conditions. We found that the effect of gene conversion is complex, and depends upon the fitness effect of gene duplication. When duplication has no effect on fitness, gene conversion accelerates the ratchet of both single-copy and duplicated genes. If duplication has an additive fitness effect, the ratchet of single-copy genes is accelerated by gene duplication, regardless of the gene conversion rate, whereas gene conversion slows the degeneration of duplicated genes. Our results suggest that the evolution of the Y chromosome involves several parameters, including the fitness effect of gene duplication by increasing dosage and gene conversion rate.


1987 ◽  
Vol 7 (4) ◽  
pp. 1559-1562
Author(s):  
J Silver ◽  
A Rabson ◽  
T Bryan ◽  
R Willey ◽  
M A Martin

Novel endogenous human retroviral sequences were cloned by low-stringency hybridization, using the pol gene of endogenous human retrovirus 51-1. One clone, lambda NP-2, contained gag, pol, env, and long terminal repeat sequences related to the corresponding portions of clone 51-1 and the closely related full-length endogenous human retrovirus 4-1. The sequence of the env gene of NP-2 was 73% homologous to that of 4-1. Genomic Southern blots of male and female DNAs showed that NP-2 is located on the Y chromosome and that the Y chromosome also contains one other sequence closely related to the env and 3' flanking regions of NP-2. Conservation of flanking DNA suggests that the second Y chromosome copy of the NP-2 env sequence arose by gene duplication rather than provirus insertion.


2017 ◽  
Vol 136 (5) ◽  
pp. 605-619 ◽  
Author(s):  
Beniamino Trombetta ◽  
Fulvio Cruciani
Keyword(s):  

1987 ◽  
Vol 7 (4) ◽  
pp. 1559-1562 ◽  
Author(s):  
J Silver ◽  
A Rabson ◽  
T Bryan ◽  
R Willey ◽  
M A Martin

Novel endogenous human retroviral sequences were cloned by low-stringency hybridization, using the pol gene of endogenous human retrovirus 51-1. One clone, lambda NP-2, contained gag, pol, env, and long terminal repeat sequences related to the corresponding portions of clone 51-1 and the closely related full-length endogenous human retrovirus 4-1. The sequence of the env gene of NP-2 was 73% homologous to that of 4-1. Genomic Southern blots of male and female DNAs showed that NP-2 is located on the Y chromosome and that the Y chromosome also contains one other sequence closely related to the env and 3' flanking regions of NP-2. Conservation of flanking DNA suggests that the second Y chromosome copy of the NP-2 env sequence arose by gene duplication rather than provirus insertion.


Genes ◽  
2011 ◽  
Vol 2 (1) ◽  
pp. 131-151 ◽  
Author(s):  
J. Roman Arguello ◽  
Tim Connallon

2004 ◽  
Vol 16 (5) ◽  
pp. 527 ◽  
Author(s):  
Jennifer A. Marshall Graves

The human Y chromosome is running out of time. In the last 300 million years, it has lost 1393 of its original 1438 genes, and at this rate it will lose the last 45 in a mere 10 million years. But there has been a proposal that perhaps rescue is at hand in the form of recently discovered gene conversion within palindromes. However, I argue here that although conversion will increase the frequency of variation of the Y (particularly amplification) between Y chromosomes in a population, it will not lead to a drive towards a more functional Y. The forces of evolution have made the Y a genetically isolated, non-recombining entity, vulnerable to genetic drift and selection for favourable new variants sharing the Y with damaging mutations. Perhaps it will even speed up the decline of the Y chromosome and the onset of a new round of sex-chromosome differentiation. The struggle to preserve males may perhaps lead to hominid speciation.


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