The Impact of Dominance on Adaptation in Changing Environments

Natural environments are seldom static and therefore it is important to ask how a population adapts in a changing environment. We consider a finite, diploid population evolving in a periodically changing environment and study how the fixation probability of a rare mutant depends on its dominance coefficient and the rate of environmental change. We find that, in slowly changing environments, the effect of dominance is the same as in the static environment, that is, if a mutant is beneficial (deleterious) when it appears, it is more (less) likely to fix if it is dominant. But, in fast changing environments, the effect of dominance can be different from that in the static environment and is determined by the mutant’s fitness at the time of appearance as well as that in the time-averaged environment. We find that, in a rapidly varying environment that is neutral on average, an initially beneficial (deleterious) mutant that arises while selection is decreasing (increasing) has a fixation probability lower (higher) than that for a neutral mutant as a result of which the recessive (dominant) mutant is favored. If the environment is beneficial (deleterious) on average but the mutant is deleterious (beneficial) when it appears in the population, the dominant (recessive) mutant is favored in a fast changing environment. We also find that, when recurrent mutations occur, dominance does not have a strong influence on evolutionary dynamics.

The impact of dominance on adaptation in changing environments

Natural environments are seldom static and therefore it is important to ask how a population adapts in a changing environment. We consider a finite, diploid population evolving in a periodically changing environment and study how the fixation probability of a rare mutant depends on its dominance coefficient and the rate of environmental change. We find that in slowly changing environments, the effect of dominance is the same as in the static environment, that is, if a mutant is beneficial (deleterious) when it appears, it is more (less) likely to fix if it is dominant. But in fast changing environments, the effect of dominance can be different from that in the static environment and is determined by the mutant’s fitness at the time of appearance as well as that in the time-averaged environment. We find that in a rapidly varying environment which is neutral on average, an initially beneficial (deleterious) mutant that arises while selection is decreasing (increasing) has a fixation probability lower (higher) than that for a neutral mutant as a result of which the recessive (dominant) mutant is favored. If the environment is beneficial (deleterious) on average but the mutant is deleterious (beneficial) when it appears in the population, the dominant (recessive) mutant is favored in a fast changing environment. We also find that when recurrent mutations occur, dominance does not have a strong influence on evolutionary dynamics.

Complexity in SARS-CoV-2 genome data: Price theory of mutant isolates

SARS-CoV-2 is a highly virulent and deadly RNA virus causing the Covid-19 pandemic and several deaths across the world. The pandemic is so fast that any concrete theory of sudden widespread of this disease is still not known. In this work, we studied and analyzed a large number of publicly available SARS-CoV-2 genomes across the world using the multifractal approach. The mutation events in the isolates obey the Markov process and exhibit very high mutational rates, which occur in six specific genes and highest in orf1ab gene, leading to virulent nature. f (α) analysis indicated that the isolates are highly asymmetric (left-skewed), revealing the richness of complexity and dominance by large fluctuations in genome structure organization. The values of Hq and Dq are found to be significantly large, showing heterogeneous genome structure self-organization, strong positive correlation in organizing the isolates, and quite sensitive to fluctuations in and around it. We then present multiple-isolates hosts-virus interaction models, and derived Price equation for the model. The phase plane analysis of the model showed asymptotic stability type bifurcation. The competition among the mutant isolates drives the trade-off of the dominant mutant isolates, otherwise confined to the present hosts.

Variation in maize chlorophyll biosynthesis alters plant architecture

Chlorophyll is a tetrapyrrole metabolite essential for photosynthesis in plants. The oil yellow1 (oy1) gene of maize encodes subunit I of Magnesium chelatase, the enzyme catalyzing the first committed step of chlorophyll biosynthesis. A range of chlorophyll contents and net CO2 assimilation rates can be achieved in maize by combining a semi-dominant mutant allele, Oy1-N1989, and cis-regulatory alleles encoded by the Mo17 inbred called very oil yellow1 (vey1). We previously demonstrated that these allelic interactions can delay reproductive maturity. In this study, we demonstrate that multiple gross morphological traits respond to a reduction in chlorophyll. We found that stalk width, number of lateral branches (tillers), and branching of the inflorescence decline with a decrease in chlorophyll level. Chlorophyll variation suppressed tillering in multiple maize mutants including teosinte branched1, grassy tiller1, and Tillering1 as well as the tiller number1 QTL responsible for tillering in many sweet corn varieties. In contrast to these traits, plant height showed a non-linear response to chlorophyll levels. Weak suppression of Oy1-N1989 by vey1B73 resulted in a significant increase in mutant plant height. This was true in multiple mapping populations, isogenic inbreds, and hybrid backgrounds. Enhancement of the Oy1-N1989 mutants by the vey1Mo17 allele reduced chlorophyll contents and plant height in mapping populations and isogenic inbred background. We demonstrate that the effects of reduced chlorophyll content on plant growth and development are complex and that the genetic relationship depends on the trait. We propose that growth control for branching and architecture are downstream of energy balance sensing.

Mapping the growth effect of previously hidden ubiquitin alleles using an overexpression based mutational scan

Deep mutational scanning has emerged as a powerful, high throughput approach to determine the growth effect of thousands of alleles at once in bulk competition. However, to date only the growth effect of mutant alleles in isolation has been determined. Building off previous work, we have created a library of all possible single point mutations in ubiquitin and determined the growth effect of mutants overexpressed in the presence of a wild type allele. Using this scan, we explained over half of the previously missing mutants in the single allele scan by showing that they exhibit deleterious effects when co-expressed with wild type ubiquitin. Additionally, unlike the single allele growth effect, these overexpression growth effects were distributed across the entire protein. This overexpression scan methodology can identify likely dominant mutant effects in any essential gene and is highly complementary with traditional deep mutational scanning approaches.

Cerebral Cavernous Malformations Develop through Clonal Expansion of Mutant Endothelial Cells

RationaleVascular malformations arise in vessels throughout the entire body. Causative genetic mutations have been identified for many of these diseases; however, little is known about the mutant cell lineage within these malformations.ObjectiveWe utilize an inducible mouse model of cerebral cavernous malformations (CCMs) coupled with a multi-color fluorescent reporter to visualize the contribution of mutant endothelial cells (ECs) to the malformation.Methods and ResultsWe combined a Ccm3 mouse model with the confetti fluorescent reporter to simultaneously delete Ccm3 and label the mutant EC with one of four possible colors. We acquired Z-series confocal images from serial brain sections and created 3D reconstructions of entire CCMs to visualize mutant ECs during CCM development. We observed a pronounced pattern of CCMs lined with mutant ECs labeled with a single confetti color (n=42). The close 3D distribution, as determined by the nearest neighbor analysis, of the clonally dominant ECs within the CCM was statistically different than the background confetti labeling of ECs in non-CCM control brain slices as well as a computer simulation (p<0.001). Many of the small (<100μm diameter) CCMs consisted, almost exclusively, of the clonally dominant mutant ECs labeled with the same confetti color whereas the large (>100μm diameter) CCMs contained both the clonally dominant mutant cells and wildtype ECs. We propose of model of CCM development in which an EC acquires a second somatic mutation, undergoes clonal expansion to initiate CCM formation, and then incorporates neighboring wildtype ECs to increase the size of the malformation.ConclusionsThis is the first study to visualize, with single-cell resolution, the clonal expansion of mutant ECs within CCMs. The incorporation of wildtype ECs into the growing malformation presents another series of cellular events whose elucidation would enhance our understanding of CCMs and may provide novel therapeutic opportunities.

Revolute-Leaf, a New Completely Dominant Mutant in Peanut

ABSTRACT A Revolute-Leaf mutant plant was discovered in an advanced Georgia peanut (Arachis hypogaea L.) breeding line, GA 112702. The mutant had leaf margins that curve downward on each of the four small light-green leaflets. Two cross combinations were used to determine the inheritance of this new mutant. F1, F2, and F3 segregation data strongly supported a single completely dominant gene, designated Rev, controlling the inheritance of the Revolute-Leaf mutant. The F2:3 homozygous revolute-leaf individual plants had shorter mainstem heights, narrower leaflet length and width, narrower canopy width, reduced pod and seed weights, but similar SMK percentages compared to the F2:3 homozygous normal leaf plants resulting from the same closely related cross combination (GA 112702 x Revoluted-Leaf mutant).