GSE168062
Transcriptional contribution of nuclear lamina protein emerin and BAF in Drosophila ovaries
Nuclear lamina (NL) contributes to tissue homeostasis. In Drosophila, compromised NL blocks differentiation and causes loss of germline stem cells (GSCs) due to activation of the Chk2 checkpoint kinase. Checkpoint activation occurs upon loss of the NL protein Drosophila emerin or its partner Barrier-to-autointegration factor (BAF). As NL has long been thought to interact with specific genomic loci and regulate transcription, we examined transcriptional changes in emerin-/- and baf KD ovaries. We found thousands of genes are mis-regulated upon loss of emerin or BAF in GSCs. Remarkably, more than 90% of mis-regulated genes are shared between emerin-/- and baf KD. Finally, we show that transcriptional changes are downstream of Chk2 activation, as transcription are restored in chk2, emerin double mutant ovaries. Overall design: Ovary mRNA profiles of newly eclosed wildtype, emerin mutant and bafKD Drosophila. G/PI and G/PK are the genotypes of the two emerin null flies. The G, PK, and PI alleles are emerin null, we used both backgrounds to control for background effects.