Abstract
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.
Highlights
Abnormalities in chromosome number have the potential to disrupt the balance of gene expression and thereby decrease organismal fitness and viability (Siegel and Amon, 2012)
Changes in chromosome number have the potential to disrupt the balance of gene expression and thereby reduce organismal fitness
Genes on the male X would be expressed at half the total level as genes on the ancestral autosomes and on the two Figure 7 continued fraction of autosomal FISH signals in each of three zones in XX or XO embryos of two age groups (50-140-cell stage or > 200-cell stage) from wild-type strains or ectopic rex-insertion strains
Summary
Abnormalities in chromosome number (aneuploidy) have the potential to disrupt the balance of gene expression and thereby decrease organismal fitness and viability (Siegel and Amon, 2012). This means that males have half the copy number (dose) of genes on the X chromosome Human cells correct this imbalance by suppressing the activity, or expression, of most of the genes on one of the X chromosomes in females. Modern sex chromosomes evolved from a pair of non-sex chromosomes, and males lost one copy of all of the genes located on those ancestral chromosomes This evolutionary history causes both sexes to have lower gene expression from X chromosomes than the other chromosomes, raising the question of whether a mechanism exists to balance out the difference in gene expression between sex chromosomes and non-sex chromosomes. These results mean that no chromosome-wide mechanism balances gene expression levels between the X chromosome and the non-sex chromosomes It remains unknown how C. elegans, and many other living organisms, evolved to tolerate a lower level of gene expression from the sex chromosomes. Step 3 (rare): prevented between pX and pY; The pY pY degrades over time chromosome is lost
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