Faculty Opinions recommendation of Experimental evolution of the genetic load and its implications for the genetic basis of inbreeding depression.

Author(s):  
Fred Allendorf
2003 ◽  
Vol 358 (1434) ◽  
pp. 1071-1084 ◽  
Author(s):  
David E. Carr ◽  
Michele R. Dudash

Predictions for the evolution of mating systems and genetic load vary, depending on the genetic basis of inbreeding depression (dominance versus overdominance, epistasis and the relative frequencies of genes of large and small effect). A distinction between the dominance and overdominance hypotheses is that deleterious recessive mutations should be purged in inbreeding populations. Comparative studies of populations differing in their level of inbreeding and experimental approaches that allow selection among inbred lines support this prediction. More direct biometric approaches provide strong support for the importance of partly recessive deleterious alleles. Investigators using molecular markers to study quantitative trait loci (QTL) often find support for overdominance, though pseudo–overdominance (deleterious alleles linked in repulsion) may bias this perception. QTL and biometric studies of inbred lines often find evidence for epistasis, which may also contribute to the perception of overdominance, though this may be because of the divergent lines initially crossed in QTL studies. Studies of marker segregation distortion commonly uncover genes of major effect on viability, but these have only minor contributions to inbreeding depression. Although considerable progress has been made in understanding the genetic basis of inbreeding depression, we feel that all three aspects merit more study in natural plant populations.


Genome ◽  
1996 ◽  
Vol 39 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Kermit Ritland

Recent progress in the genetic analysis of inbreeding depression in plants is reviewed. While the debate over the importance of genes of dominance versus overdominance effect continues, the scope of inferences has widened and now includes such facets as the interactions between genes, the relative abundance of major versus minor genes, life cycle stage expression, and mutation rates. The types of inferences are classified into the genomic, where many genes are characterized as an average, and the genic, where individual genes are characterized. Genomic inferences can be based upon natural levels of inbreeding depression, purging experiments, the comparison of individuals of differing F (e.g., prior inbreeding), and various crossing designs. Genic inferences mainly involve mapping and characterizing loci with genetic markers, involving either a single cross or, ideally, several crosses. Alternative statistical models for analyzing polymorphic loci causing inbreeding depression should be a fruitful problem for geneticists to pursue. Key words : inbreeding depression, genetic load, self-fertilization, QTL mapping.


Heredity ◽  
2013 ◽  
Vol 112 (3) ◽  
pp. 248-254 ◽  
Author(s):  
I M Chelo ◽  
S Carvalho ◽  
M Roque ◽  
S R Proulx ◽  
H Teotónio

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Alexey A. Grum-Grzhimaylo ◽  
Eric Bastiaans ◽  
Joost van den Heuvel ◽  
Cristina Berenguer Millanes ◽  
Alfons J. M. Debets ◽  
...  

AbstractSome multicellular organisms can fuse because mergers potentially provide mutual benefits. However, experimental evolution in the fungus Neurospora crassa has demonstrated that free fusion of mycelia favours cheater lineages, but the mechanism and evolutionary dynamics of this exploitation are unknown. Here we show, paradoxically, that all convergently evolved cheater lineages have similar fusion deficiencies. These mutants are unable to initiate fusion but retain access to wild-type mycelia that fuse with them. This asymmetry reduces cheater-mutant contributions to somatic substrate-bound hyphal networks, but increases representation of their nuclei in the aerial reproductive hyphae. Cheaters only benefit when relatively rare and likely impose genetic load reminiscent of germline senescence. We show that the consequences of somatic fusion can be unequally distributed among fusion partners, with the passive non-fusing partner profiting more. We discuss how our findings may relate to the extensive variation in fusion frequency of fungi found in nature.


Evolution ◽  
1999 ◽  
Vol 53 (5) ◽  
pp. 1354-1365 ◽  
Author(s):  
Katri Kärkkäinen ◽  
Helmi Kuittinen ◽  
Rob van Treuren ◽  
Claus Vogl ◽  
Sami Oikarinen ◽  
...  

2000 ◽  
Vol 75 (1) ◽  
pp. 75-81 ◽  
Author(s):  
THOMAS BATAILLON ◽  
MARK KIRKPATRICK

We studied the effects of population size on the inbreeding depression and genetic load caused by deleterious mutations at a single locus. Analysis shows how the inbreeding depression decreases as population size becomes smaller and/or the rate of inbreeding increases. This pattern contrasts with that for the load, which increases as population size becomes smaller but decreases as inbreeding rate goes up. The depression and load both approach asymptotic limits when the population size becomes very large or very small. Numerical results show that the transition between the small and the large population regimes is quite rapid, and occurs largely over a range of population sizes that vary by a factor of 10. The effects of drift on inbreeding depression may bias some estimates of the genomic rate of deleterious mutation. These effects could also be important in the evolution of breeding systems in hermaphroditic organisms and in the conservation of endangered populations.


Author(s):  
Juan-Vicente Bou ◽  
Rafael Sanjuán

Abstract Many animal viruses replicate and are released from cells in close association to membranes. However, whether this is a passive process or is controlled by the virus remains poorly understood. Importantly, the genetic basis and evolvability of membrane-associated viral shedding have not been investigated. To address this, we performed a directed evolution experiment using coxsackievirus B3, a model enterovirus, in which we repeatedly selected the free-virion or the fast-sedimenting membrane-associated viral subpopulations. The virus responded to this selection regime by reproducibly fixing a series of mutations that altered the extent of membrane-associated viral shedding, as revealed by full-genome ultra-deep sequencing. Specifically, using site-directed mutagenesis, we showed that substitution N63H in the viral capsid protein VP3 reduced the ratio of membrane-associated to free viral particles by 2 orders of magnitude. These findings open new avenues for understanding the mechanisms and implications of membrane-associated viral transmission.


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