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Drosophila  wings mainly consist of two cell types, vein and intervein cells. Acquisition of either fate depends on specific expression of genes that are controlled by several signaling pathways. The nuclear mechanisms that translate signaling into regulation of gene expression are not completely understood, but they involve chromatin factors from the Trithorax (TrxG) and Enhancers of Trithorax and Polycomb (ETP) families. One of these is the ETP Corto that participates in intervein fate through interaction with the  Drosophila  EGF Receptor – MAP kinase ERK pathway. Precise mechanisms and molecular targets of Corto in this process are not known. We show here that Corto interacts with the Elongin transcription elongation complex. This complex, that consists of three subunits (Elongin A, B, C), increases RNA polymerase II elongation rate  in vitro  by suppressing transient pausing. Analysis of phenotypes induced by  EloA ,  B , or  C  deregulation as well as genetic interactions suggest that the Elongin complex might participate in vein  vs  intervein specification, and antagonizes  corto  as well as several TrxG genes in this process. Chromatin immunoprecipitation experiments indicate that Elongin C and Corto bind the vein-promoting gene  rhomboid  in wing imaginal discs. We propose that Corto and the Elongin complex participate together in vein  vs  intervein fate, possibly through tissue-specific transcriptional regulation of  rhomboid .

The Elongin Complex Antagonizes the Chromatin Factor Corto for Vein versus Intervein Cell Identity in Drosophila Wings