The cellular basis of hybrid dysgenesis and Stellate regulation in Drosophila

Curr Opin Genet Dev. 2015 Oct:34:88-94. doi: 10.1016/j.gde.2015.09.003. Epub 2015 Oct 24.

Abstract

During normal tissue development, the accumulation of unrepaired cellular and genomic damage can impair growth and ultimately leads to death. To preserve cellular integrity, cells employ a number of defense mechanisms including molecular checkpoints, during which development is halted while dedicated pathways attempt repair. This process is most critical in germline tissues where cellular damage directly threatens an organism's reproductive capacity and offspring viability. In the fruit fly, Drosophila melanogaster, germline development has been extensively studied for over a century and the breadth of our knowledge has flourished in the genomics age. Intriguingly, several peculiar phenomena that trigger catastrophic germline damage described decades ago, still endure only a partial understanding of the underlying molecular causes. A deeper reexamination using new molecular and genetic tools may greatly benefit our understanding of host system biology. Among these, and the focus of this concise review, are hybrid dysgenesis and an intragenomic conflict that pits the X and Y sex chromosomes against each other.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Drosophila Proteins / genetics*
  • Drosophila melanogaster / genetics
  • Drosophila melanogaster / growth & development*
  • Germ Cells / growth & development*
  • Germ Cells / metabolism
  • Germ Cells / pathology
  • Gonadal Dysgenesis / genetics*
  • Gonadal Dysgenesis / pathology
  • Protein Kinases / genetics*
  • Sex Chromosomes / genetics
  • Systems Biology

Substances

  • Drosophila Proteins
  • Protein Kinases
  • Ste protein, Drosophila