Drivers of achiasmatic meiosis: sexual antagonism versus heteromorphy-dependent aneuploidy across sex-chromosome divergence.
Summary
Ingested 2026-04-21. 3 findings extracted and verified.
Findings worth citing
Finding 1 — Achiasmy-causing mutations fix most readily on the Y chromosome under sexual antagonism, reaching equilibrium ~4× faster than on the X and ~18× faster than on autosomes.
Y chromosomes have a higher tendency to fix these mutations across the studied parameter space and do so with faster dynamics, reaching equilibrium 4 times faster than when the mutation is on the X chromosome and 18 times faster than when it is on an autosome under the same parameters
Why this is citable: Provides a quantitative prediction about the genomic distribution of achiasmy-causing mutations, useful for citing when discussing why Y chromosomes disproportionately harbor meiosis-modifying variants.
Counter / limitation: This is a deterministic population-genetic model result with specific parameter assumptions (e.g., fixed μ, δ, symmetric fitness), so the exact fold-differences may not translate to finite populations or alternate dominance/linkage regimes.
Topics: sex_chromosome_evolution, fragile_y_hypothesis
Finding 2 — The primary selective force driving achiasmy shifts across sex-chromosome divergence, with sexual antagonism dominating in young homomorphic systems and heteromorphy-dependent aneuploidy dominating in highly diverged systems.
sexually antagonistic selection is more likely to drive achiasmy in young, homomorphic sex chromosomes, whereas heteromorphy-dependent aneuploidy becomes the primary force in highly diverged, heteromorphic sex chromosomes
Why this is citable: This is the paper’s central synthesizing claim that unifies competing hypotheses for achiasmy evolution, directly citable when discussing why different taxa may have evolved achiasmy for different reasons.
Counter / limitation: The prediction relies on unspecified functional forms of SA(L,s,h) and k(L); the authors acknowledge that exact functional forms are unknown, making this a theoretically motivated hypothesis rather than empirically validated.
Topics: sex_chromosome_evolution, fragile_y_hypothesis
Finding 3 — Under heteromorphy-dependent aneuploidy selection, autosomes permit broader invasion of achiasmy mutations than X chromosomes because of higher male residence time.
the parameter space permitting invasion of this mutation is broader on autosomes than on the X chromosome, likely because autosomes reside in males half the time, whereas X chromosomes do so only one–third of the time, yielding different responses to sex–specific selection
Why this is citable: Under heteromorphy-dependent aneuploidy selection, the model shows that autosomes permit invasion of achiasmy mutations across a broader parameter space than X chromosomes, despite Y chromosomes being most permissive overall. The paper attributes this counterintuitive autosome > X ordering to residence time in males (autosomes 1/2, X chromosomes 1/3), providing a testable prediction that distinguishes the aneuploidy hypothesis from the sexual antagonism hypothesis, under which X chromosomes outrank autosomes.
Counter / limitation: The residence-time explanation assumes that the sole driver of the autosome > X ordering is male exposure frequency, but the model also differs between these genomic regions in ploidy and linkage structure; the paper does not formally isolate residence time as the sole cause, so the attributed mechanism remains an inference rather than a proven result.
Topics: sex_chromosome_evolution, fragile_y_hypothesis
Read the paper
doi.org/10.1093/g3journal/jkaf217
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