Indigenous knowledge: an inexhaustible "information bank" for toxin research.
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Animals↗
Biomedical subjects
H Huai
Publications and source records attributed to H Huai.
Transposable DNA elements and life history traits: II. Transposition of P DNA elements in somatic cells reduces fitness, mating activity, and locomotion of Drosophila melanogaster.
Some transposable DNA elements in higher organisms are active in somatic cells, as well as in germinal cells. What effect does the movement of DNA elements in somatic cells have on life history traits? It has previously been reported that somatically active P and mariner elements in Drosophila induce genetic damage and significantly reduce lifespan. In this study, we report that the movement of P elements in somatic cells also significantly reduces fitness, mating activity, and locomotion of Drosophila melanogaster. If other elements cause similar changes in life history traits, it is doubtful if transposable DNA elements remain active for long in somatic cells in natural populations.
Animals↗
Mutation rate: a simple concept has become complex.
The factors that cause new mutations or affect the rate at which they occur have important implications for many areas of genetics. But recent work on phenomena such as premeiotic mutations, which yield a cluster of identical new mutants at the some time, led us to realize that researchers are using the term "mutation rate" in different, and sometimes contradictory, ways. One premeiotic genetic change may ultimately yield several new mutant offspring, but should this be considered one new mutation or many? The way the data are handled in analyses can have a significant effect on the results. How, then, does one handle clusters in the estimation of mutation rates? We explore this question and propose that geneticists begin to distinguish clearly between three different phenomena that to this point have been given the same name: the initial prerepair "genetic damage rate," the postrepair "mutational event rate," and the observed "mutation rate" as it is expressed in the proportion of new mutant offspring. We believe that all new mutant offspring should be counted when estimating mutation rate, irrespective of when in the developmental cycle it is believed that the initial mutational event occurred.
Animals↗
With the correct concept of mutation rate, cluster mutations can explain the overdispersed molecular clock.
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Animals↗
Clusters of new identical mutants and the fate of underdominant mutations.
Given favorable environmental and demographic conditions, premeiotic clusters of identical mutations can produce a broad distribution of the initial frequency of underdominant alleles. Because of these clusters, new underdominant mutations may not necessarily be as rare in a population as previously assumed. The fixation of underdominant mutations, especially those with low heterozygous fitness, is increased when mutations appear in a cluster due to a genetic change that occurred before germline differentiation. Most restrictions on the fixation of underdominant mutations in a single population, such as strong genetic drift, weak selection against mutant heterozygotes, isolated population structure, inbreeding, meiotic drive, and selection in favor of mutant homozygotes can be relaxed or even dropped. Instead, the fate of strong underdominant mutations is determined mainly by ecological and genetic factors that affect the cluster size distribution of new premeiotic mutations. Accumulation of reproductive isolation by the fixation of underdominant mutations becomes more feasible with clusters, and mutation is not always the weakest force during this evolutionary process. The large mean and variance of reproductive success in many multicellular species make it possible that even underdominant mutations with very low heterozygous fitness could contribute substantially to reproductive isolation.
Alleles↗
Clusters of identical new mutations can account for the "overdispersed" molecular clock.
Germ-cell mutations may occur during meiosis, giving rise to independent mutant gametes in a Poisson process, or before meiosis, giving rise to multiple copies of identical mutant gametes at a much higher probability than the Poisson expectation. We report that the occurrence of these early premeiotic clusters of new identical mutant alleles increases the variance-to-mean ratio of mutation rate (R(u) > 1). This leads to an expected variance-to-mean ratio (R(t)) of the molecular clock that is always greater than one and may cover the observed range of R(t) values. Hence, the molecular clock may not be over-dispersed based on this new mutational model that includes clusters. To get a better estimation of R(u) and R(t), one needs measurements of the intrageneration variation of reproductive success (Nt/Ne(i)), population dynamics (ki), and the proportion of new mutations that occur in clusters (rc), especially those formed before germ-cell differentiation.
Animals↗
Clusters of identical new mutation in the evolutionary landscape.
In contrast to the common assumption that each new mutant results from a unique, independent mutation event, clusters of identical premeiotic mutant alleles are common. Clusters can produce large numbers of related individuals carrying identical copies of the same new genetic change. By entering the gene pool in multiple copies at one time, clusters can influence fundamental processes of population genetics. Here we report evidence that clusters can increase the arrival and fixation probabilities and can lengthen the average time to extinction of new mutations. We also suggest it may be necessary to reconsider other fundamental elements of population genetic theory.
Animals↗