Innovative use of the C.elegans model in diverse research fields

The Xue Laboratory was founded in the fall of 1997 with the express goal of studying the genetic and molecular mechanisms of programmed cell death. The laboratory has made numerous important contributions not just to the field of programmed cell death, but has extended its reach to several diverse research fields. The Xue Lab has recently redirected its focus to four major research areas: study of the genetics and molecular mechanisms that establish and maintain phospholipid asymmetry, characterization of the mechanisms and physiological significance of maternal mitochondrial inheritance during early development, analysis of radiation-induced bystander effects (RIBE) and its importance and applications in radiotherapy, and the use of C. elegans as an animal model to study various human disease and to perform drug discovery. In these pursuits the lab has very recently made significant contributions to our understanding of the mechanism of action of Hepatitis B Virus X protein, made key discoveries in the field of phosphotidylserine asymmetry and externalization (see below video). Beyond these contributions the Xue Lab has also made important discoveries in characterizing the chromosome fragmentation process during apoptosis, including the identification of the caspase-dependent conversion of the dicer ribonuclease into a deoxyribonuclease and multiple apoptotic nucleases involved in the process. We hope to continue to provide contributions to a wide array of research fields. For more detailed information about the projects studied by the Xue Lab, please see our Projects page. To contact the Xue Lab, please proceed to the Contact page.

Analysis of activation, execution, and engulfment in C. elegans embryo apoptosis

A secreted Annexin GFP sensor labels surface-exposed PS during apoptosis.

 

Analysis of paternal mitochondria elimination in a wild-type C. elegans embryo

MitoTracker Red-stained paternal mitochondria are eliminated during early embryogenesis.