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Mittell, E. A.

Publications and source records attributed to Mittell, E. A..

3 recordsLinked to original sources

Nucleotide diversity is a poor predictor of short-term adaptive potential

Significance statementThe current paradigm in conservation genetics suggests that species with the lowest molecular genetic diversity have the lowest capacity to adapt. Despite previous concern that traditional measures of molecular genetic variation are not useful predictors of adaptive potential, the conflation of genetic diversity and adaptive potential remains prevalent in both scientific literature and global policy. By combining new theory with a large dataset of genetic variation across hundreds of species, we show that molecular sequence variation is weakly related to the level of heritable variation in traits across species. This demonstrates that genetic diversity does not reliably predict adaptive potential, and highlights the urgent need to move beyond simple measures when assessing the evolutionary resilience of populations. A capacity to adapt is essential for a population to avoid extinction in a changing world and is recognised as a global conservation priority. Adaptation requires additive (heritable) genetic variation for traits that influence survival and fecundity, but measuring this variation is difficult, particularly in species of conservation concern. Instead, molecular genetic diversity is often used to infer adaptive potential. However, previous research has cast doubt on the suitability of traditional molecular markers (allozymes and microsatellites) for this purpose given their weak relationship with heritability - a common measure of additive genetic variance. Recent advances in sequencing technology have since shifted focus towards nucleotide diversity and variation in functional regions, but their practicality for predicting adaptive potential remains debated and untested. Furthermore, heritability itself is a poor proxy for adaptive potential because it depends on environmental variance. We collated 2,113 published estimates of evolvability - a measure of additive genetic variance that avoids environmental confounding - across 193 eukaryotic species, and evaluated how well evolvability is predicted by molecular diversity. We find that microsatellite and nucleotide diversity are not significantly correlated to each other, and neither predict evolvability (nucleotide diversity explains 0.7% of interspecific differences in evolvability and doubling nucleotide diversity only corresponds to a 9.2% increase in evolvability). With new theoretical work, we show that such weak associations are expected. Together, our results suggest that simple molecular measures of genetic variation are insufficient for predicting adaptive potential and continued reliance on these metrics risks misinforming conservation management.

evolutionary biology↗

The missing fraction problem as an episodes of selection problem

In evolutionary quantitative genetics, the missing fraction problem refers to the case where phenotypes seen later in life are biased because a non-random subset of those phenotypes are missing from the population due to prior viability selection on correlated traits. As any such missing fraction will bias our estimates of selection, and therefore, responses to selection, it is one potential explanation for the paradox of stasis seen in wild populations. The two components required for the missing fraction problem to arise are: (1) viability selection; and (2) correlation between later-life traits and those important for early-life survival. Although it is plausible that these conditions are widespread in wild populations, this problem has received very little attention since it was first discussed (Grafen 1988; Hadfield 2008). It is impossible to know what phenotypes would have been expressed later in life by individuals who died during an earlier episode of viability selection, which has probably put researchers off. Here we show that we can break the problem down into episodes of selection and recover either (a) true estimates of phenotypic selection for later-life traits, or (b) adjusted estimates of the response to selection, depending on the data available. Implementation of complex statistics should uncover how prevalent the problem may be across many existing datasets (the latter approach). Whereas overall, we hope that viewing the missing fraction problem as an episodes of selection problem increases motivation, and provides justification, for a shift in focus to directly studying early-life viability selection. "...what a correlation with [lifetime reproductive success] or its components tells you depends on the causes of the natural variation in the character. It will not always be easy to discover those causes." -- Grafen (1988) "It is surprising that the problem of missing data has received so little attention given that viability selection is central to evolutionary biology." -- Hadfield (2008)

evolutionary biology↗

A synthesis of senescence predictions for indeterminate growth, and support from multiple tests in wild lake trout

Senescence, or the deterioration of functionality with age, varies widely across taxa in pattern and rate. Insights into why and how this variation occurs are hindered by the predominance of lab-focused research on short-lived model species with determinate growth. We synthesize evolutionary theories of senescence, highlight key information gaps, and clarify predictions for species with low mortality and variable degrees of indeterminate growth. Lake trout are an ideal species to evaluate predictions in the wild. We monitored individual males from two populations (1976-2017) longitudinally for changes in adult mortality (actuarial senescence) and body condition (proxy for energy balance). A cross-sectional approach (2017) compared young (ages 4-10 years) and old (18-37 years) adults for (1) phenotypic performance in body condition, and semen quality - which is related to fertility under sperm competition (reproductive senescence), and (2) relative telomere length (potential proxy for cellular senescence). Adult growth in these particular populations is constrained by a simplified food web, and our data support predictions of negligible senescence when maximum size is only slightly larger than maturation size. Negative senescence (aka reverse senescence) may occur in other lake trout populations where diet shifts allow maximum sizes to be much larger than maturation size.

evolutionary biology↗