Differential effect of aneuploidy on the X chromosome and genes with sex-biased expression in Drosophila.
Global analysis of gene expression via RNA sequencing was conducted for trisomics for the left arm of chromosome 2 (2L) and compared with the normal genotype. The predominant response of genes on 2L was dosage compensation in that similar expression occurred in the trisomic compared with the diploid control. However, the male and female trisomic/normal expression ratio distributions for 2L genes differed in that females also showed a strong peak of genes with increased expression and males showed a peak of reduced expression relative to the opposite sex. For genes in other autosomal regions, the predominant response to trisomy was reduced expression to the inverse of the altered chromosomal dosage (2/3), but a minor peak of increased expression in females and further reduced expression in males were also found, illustrating a sexual dimorphism for the response to aneuploidy. Moreover, genes with sex-biased expression as revealed by comparing amounts in normal males and females showed responses of greater magnitude to trisomy 2L, suggesting that the genes involved in dosage-sensitive aneuploid effects also influence sex-biased expression. Each autosomal chromosome arm responded to 2L trisomy similarly, but the ratio distributions for X-linked genes were distinct in both sexes, illustrating an X chromosome-specific response to aneuploidy.
Division of Biological Sciences, University of Missouri, Columbia, MO 65211-7400.
Lin
L
Sun
Adam F
AF
Johnson
Jilong
J
Li
Aaron S
AS
Lambdin
Jianlin
J
Cheng
James A
JA
Birchler
D000818:Animals; D004303:Dosage Compensation, Genetic / Q000235:genetics*; D004330:Drosophila / Q000235:genetics* / Q000378:metabolism; D019143:Evolution, Molecular; D005260:Female; D063990:Gene Ontology; D007814:Larva / Q000378:metabolism; D008297:Male; D008957:Models, Genetic; D017423:Sequence Analysis, RNA; D012727:Sex Characteristics; D014314:Trisomy; D014960:X Chromosome / Q000235:genetics*
autosomal dosage compensation; dot chromosome; gene balance hypothesis; inverse effect; sex chromosome evolution