Muller's ratchet

Without directed evolution, he said, a basic principle of genetics, known as Muller's ratchet, takes over.

This is known as Muller's ratchet.

It is not easy to ascribe cases of genome shrinkage or fast evolution to Muller's ratchet alone.

Continued fixation of deleterious alleles in small populations is called Muller's ratchet, and can lead to mutational meltdown.

Muller's ratchet is the gradual, but irreversible accumulation of deleterious mutations in asexual organisms.

Fitness of RNA virus decreased by Muller's ratchet.

Muller's ratchet (genetics)

This incapability of the endosymbiotic bacteria to reinstate its wild type phenotype via a recombination process is called as Muller's ratchet phenomenon.

Muller's ratchet phenomenon together with less effective population sizes has led to an accretion of deleterious mutations in the non-essential genes of the intracellular bacteria.

In this manner, the organism bypasses "Muller's ratchet," the process by which the genomes of an asexual population accumulate deleterious mutations in an irreversible manner.

The effects of Muller's ratchet in the maternal complement in these hybrid offspring may therefore be masked to some extent by wild-type alleles in the paternal complement.

In contrast, the genomes of mitochondria and chloroplasts do not recombine and would undergo Muller's ratchet were they not as small as they are (see Birdsell and Wills [pp.

Muller first introduced the term "ratchet" in his 1964 paper, and the phrase "Muller's ratchet" was coined by Joe Felsenstein in his 1974 paper, "The Evolutionary Advantage of Recombination".

Because Muller's ratchet relies on genetic drift, it turns faster in smaller populations and it is thought to set limits to the maximum size of asexual genomes and to the long-term evolutionary continuity of asexual lineages.

Although Muller's ratchet is proposed to explain the success of sexual reproduction over asexual reproduction, the negative effect of accumulating irreversible deleterious mutations may not be prevalent in organisms which, while they reproduce asexually, also undergo other forms of genetic recombination.

In sexually reproducing organisms non-recombining chromosomes or chromosomal regions such as the mammalian Y chromosome (with the exception of multi-copy sequences which do engage intrachromosomal recombination and gene conversion), should also be subject to the effects of Muller's ratchet.

Even in a large population, very few individuals may be free of any deleterious mutations; if this fittest class fails to leave descendents, it can never be recovered, and the mean fitness of the population will decline irreversibly, in a process known as 'Muller's ratchet'.

In multicellular organisms that reproduce asexually through a single-cell stage, the effects of Muller's ratchet will be exacerbated, both because population sizes tend to be smaller than for protozoans, and because genomes tend to be large and hence to accumulate more mutations per genome.

The repeat random loss of well-adapted Y chromosomes, coupled with the tendency of the Y chromosome to evolve to have more deleterious mutations rather than less for reasons described above, contributes to the species-wide degeneration of Y chromosomes through Muller's ratchet.

Φ6 has been studied as a model to understand how segmented RNA viruses package their genomes, its structure has been studied by scientists interested in lipid-containing bacteriophages, and it has been used as a model organism to test evolutionary theory such as Muller's ratchet.

The shuffling of genes brought about by genetic recombination is thought to have many advantages, as it is a major engine of genetic variation and also allows sexually reproducing organisms to avoid Muller's ratchet, in which the genomes of an asexual population accumulate deleterious mutations in an irreversible manner.