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.


Nature ◽  
1995 ◽  
Vol 375 (6527) ◽  
pp. 111-112 ◽  
Author(s):  
Leo W. Beukeboom ◽  
Rolf P. Weinzierl ◽  
Nico K. Michiels

1999 ◽  
Vol 73 (4) ◽  
pp. 2745-2751 ◽  
Author(s):  
Eloisa Yuste ◽  
Sonsoles Sánchez-Palomino ◽  
Concha Casado ◽  
Esteban Domingo ◽  
Cecilio López-Galíndez

ABSTRACT Muller’s ratchet predicts fitness losses in small populations of asexual organisms because of the irreversible accumulation of deleterious mutations and genetic drift. This effect should be enhanced if population bottlenecks intervene and fixation of mutations is not compensated by recombination. To study whether Muller’s ratchet could operate in a retrovirus, 10 biological clones were derived from a human immunodeficiency virus type 1 (HIV-1) field isolate by MT-4 plaque assay. Each clone was subjected to 15 plaque-to-plaque passages. Surprisingly, genetic deterioration of viral clones was very drastic, and only 4 of the 10 initial clones were able to produce viable progeny after the serial plaque transfers. Two of the initial clones stopped forming plaques at passage 7, two others stopped at passage 13, and only four of the remaining six clones yielded infectious virus. Of these four, three displayed important fitness losses. Thus, despite virions carrying two copies of genomic RNA and the system displaying frequent recombination, HIV-1 manifested a drastic fitness loss as a result of an accentuation of Muller’s ratchet effect.


1992 ◽  
Vol 89 (13) ◽  
pp. 6015-6019 ◽  
Author(s):  
E. Duarte ◽  
D. Clarke ◽  
A. Moya ◽  
E. Domingo ◽  
J. Holland

Evolution ◽  
2004 ◽  
Vol 58 (7) ◽  
pp. 1403 ◽  
Author(s):  
Doris Bachtrog ◽  
Isabel Gordo

The Lancet ◽  
2004 ◽  
Vol 364 (9441) ◽  
pp. 1213
Author(s):  
Keith Baverstock

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