L16 sex linkage in speciation Flashcards
How do effective population sizes (Ne) compare for autosomes, X chromosomes, and Y/W chromosomes in a diploid, equal‐sex species?
Autosomes: 2N copies (Ne=A); X: 1.5N copies → Ne_X ≈¾Ne_A; Y/W: 0.5N copies → Ne_Y/W ≈¼Ne_A.
What are the consequences of reduced Ne on sex chromosomes?
Stronger genetic drift accelerates fixation or loss of alleles, reduces standing variation, and can override weak selection (especially on Y/W).
What causes male‐biased mutation and how do rates differ among chromosomes?
Spermatogenesis involves ≫24 germ‐cell divisions versus ~24 in oogenesis, leading to more replication errors in males. Thus mutation rates rank Y > Z > A > X > W.
Give experimental evidence for male mutation bias.
Human–chimpanzee sequence comparisons show Y substitutions highest, autosomal intermediate, X lowest (approx. 1.2× autosome for Y; Drost & Lee 1995).
Define heterochiasmy and its evolutionary impact.
Sex differences in recombination rates (e.g., human female rate ~1.6× male). On X/Z, recombination only in homogametic sex; none on Y/W, promoting gene loss via Muller’s ratchet.
Outline how recombination suppression leads to Y‐chromosome degeneration.
Successive inversions block crossing‐over, preventing removal of deleterious mutations; pseudogenization and gene loss accumulate over time.
What is hemizygosity and why does it matter for selection on X/Z?
In XY/ZW individuals, X/Z loci have a single copy, exposing recessive alleles directly to selection—purging deleterious and fixing beneficial variants faster.
Describe the “fast X” effect and its theoretical basis.
When beneficial mutations are recessive (low dominance h), hemizygosity on X unshields them, so adaptive substitution rate k_X > k_A under h < 0.5 (Charlesworth et al. 1987).
Provide empirical support for the fast X effect.
Drosophila experimental evolution shows higher X‐linked vs. autosomal divergence at amino‐acid sites consistent with recessive beneficials (Mank et al. 2010).
What is sexual antagonism?
Genetic conflict where alleles benefit one sex but harm the other; e.g., an allele increasing female fecundity but reducing male mating success.
How does sexual antagonism shape chromosomal distributions of alleles?
Female‐beneficial/male‐detrimental alleles accumulate on X (more time in females); male‐beneficial/female‐detrimental on Y (exclusive to males).
What are compensatory modifiers and how do they evolve?
Unlinked genes that mitigate harmful effects of a sex‐linked allele in the disadvantaged sex; theory predicts X‐linked compensators often fix more readily when harm is female‐biased.
Summarize a model predicting whether X or autosomes evolve faster.
Under equal sex selection/mutation and h<0.5, k_X>k_A (“fast X”). If h>0.5 (dominant), autosomes may adapt faster. Extensions include male mutation bias and skewed sex ratios.
Explain why overall recombination is lower on X/Z than autosomes.
X/Z only recombine in homogametic sex; autosomes recombine in both—resulting in larger linkage blocks on X/Z and stronger background selection.
List the five most critical concepts from Part 1.
(1) Ne differences (X=¾, Y/W=¼ of autosome), (2) male mutation bias, (3) heterochiasmy & recombination suppression, (4) hemizygosity exposing recessives, (5) sexual antagonism & fast X.
How is the fast X effect empirically tested using dN/dS ratios?
By plotting each gene’s nonsynonymous/synonymous substitution rate on the X (dN/dS_X) against its rate on autosomes (dN/dS_A); points above the diagonal indicate faster X evolution, a pattern seen in Drosophila, mammals, and birds.
What is the McDonald–Kreitman (MK) test and how does it estimate the proportion of adaptive substitutions (α)?
The MK test compares fixed differences (dN, dS) between species with polymorphisms (Pn, Ps) within species in a 2×2 table; a significant excess of dN relative to Pn yields α = 1 – (dS·Pn)/(dN·Ps), estimating the fraction of substitutions driven by positive selection.
What does a higher α on X-linked genes versus autosomal genes imply?
That a greater fraction of X-linked substitutions are adaptive, reinforcing the fast X hypothesis by distinguishing adaptive from neutral divergence.
How do transcriptome-based divergence analyses support faster X evolution?
By using RNA-seq to compare between‐species expression divergence to within‐species variance for each chromosome arm and applying G tests; the X often shows disproportionately high expression divergence.
State Haldane’s Rule in evolutionary genetics.
“When in the F₁ offspring of two different animal species one sex is absent, rare, or sterile, that sex is the heterogametic sex” (XY males in mammals/Drosophila; ZW females in birds/butterflies).
What is the Large X Effect (LXE) in speciation?
The phenomenon where replacing one species’ X chromosome with another’s causes a larger decline in hybrid fitness than substituting a similarly sized autosome.
Describe the dominance theory explanation for Haldane’s Rule.
Recessive incompatibility alleles on the X are exposed in the hemizygous sex, causing inviability or sterility in hybrids of the heterogametic sex.
Name and briefly reject two alternative hypotheses for Haldane’s Rule besides dominance theory.
(1) Fragile‐Male Hypothesis (male gametogenesis sensitivity)—fails in ZW systems; (2) Genetic Imbalance (X:A dosage imbalance)—invalidated by attached‐X experiments.
What was the objective and result of the attached X cross in Drosophila?
To test if X:autosome dosage imbalance caused male‐specific hybrid inviability by creating phenotypic females with an unbalanced attached X; hybrids were viable, rejecting dosage imbalance as the sole cause.
