Chromosome-wide mechanisms to decouple gene expression from gene dose during sex-chromosome evolution

Bayly S. Wheeler, Erika Anderson, Christian Frøkjær-Jensen, Qian Bian, Erik Jorgensen, Barbara J. Meyer*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


Changes in chromosome number impair fitness by disrupting the balance of gene expression. Here we analyze mechanisms to compensate for changes in gene dose that accompanied the evolution of sex chromosomes from autosomes. Using single-copy transgenes integrated throughout the Caenorhabditis elegans genome, we show that expression of all X-linked transgenes is balanced between XX hermaphrodites and XO males. However, proximity of a dosage compensation complex (DCC) binding site (rex site) is neither necessary to repress X-linked transgenes nor sufficient to repress transgenes on autosomes. Thus, X is broadly permissive for dosage compensation, and the DCC acts via a chromosome-wide mechanism to balance transcription between sexes. In contrast, no analogous X-chromosome-wide mechanism balances transcription between X and autosomes: expression of compensated hermaphrodite X-linked transgenes is half that of autosomal transgenes. Furthermore, our results argue against an X-chromosome dosage compensation model contingent upon rex-directed positioning of X relative to the nuclear periphery.

Original languageEnglish (US)
Article numbere17365
Issue numberAUGUST
StatePublished - Aug 30 2016
Externally publishedYes

Bibliographical note

Publisher Copyright:
© Wheeler et al.

ASJC Scopus subject areas

  • General Immunology and Microbiology
  • General Biochemistry, Genetics and Molecular Biology
  • General Neuroscience


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