Bar Represses dPax2 and Decapentaplegic to Regulate Cell Fate and Morphogenetic Cell Death in Drosophila Eye

Abstract

The coordinated regulation of cell fate and cell survival is crucial for normal pattern formation in developing organisms. In Drosophila compound eye development, crystalline arrays of hexagonal ommatidia are established by precise assembly of diverse cell types, including the photoreceptor cells, cone cells and interommatidial (IOM) pigment cells. The molecular basis for controlling the number of cone and IOM pigment cells during ommatidial pattern formation is not well understood. Here we present evidence that BarH1 and BarH2 homeobox genes are essential for eye patterning by inhibiting excess cone cell differentiation and promoting programmed death of IOM cells. Specifically, we show that loss of Bar from the undifferentiated retinal precursor cells leads to ectopic expression of Prospero and dPax2, two transcription factors essential for cone cell specification, resulting in excess cone cell differentiation. We also show that loss of Bar causes ectopic expression of the TGFβ homolog Decapentaplegic (Dpp) posterior to the morphogenetic furrow in the larval eye imaginal disc. The ectopic Dpp expression is not responsible for the formation of excess cone cells in Bar loss-of-function mutant eyes. Instead, it causes reduction in IOM cell death in the pupal stage by antagonizing the function of pro-apoptotic gene reaper. Taken together, this study suggests a novel regulatory mechanism in the control of developmental cell death in which the repression of Dpp by Bar in larval eye disc is essential for IOM cell death in pupal retina.

A transposable element insertion is associated with an alternative life history strategy

“…Additionally we observed enrichment of ‘MAP kinase activity’ (GO:0004709, p = 0.00109) in genes downregulated within Alba wings. In Drosophila , BarH-1 represses Decapentaplegic, a morphogen that is homolog to TGFβ 38 . TGFβ can activate signalling cascades, including MAP kinase pathways 39 .…”

Angiotensin-converting enzyme Ance is cooperatively regulated by Mad and Pannier in Drosophila imaginal discs

“…Although Ance null mutants do not exhibit obvious developmental defects, it is important to note that loss of Ance can modulate the phenotypes of impaired Dpp signaling. It has been shown that overexpression of dpp by GMR - Gal4 causes severe roughness and bulging of the adult eye 46 . We showed that reduced Ance partially suppressed the effects of Dpp overexpression (Fig.…”

Rationally-engineered reproductive barriers using CRISPR & CRISPRa: an evaluation of the synthetic species concept inDrosophila melanogaster

“…By comparison, the sgRNAs for dpp4, dpp5, engrailed, hairy, hid1, hid2, rad51, reaper2 increased the expression of their target genes at more moderate levels ( Figure 2B). The sgRNAs dpp1, dpp2, dpp3 and reaper2 were found to suppress gene expression compared to contols, possibly due to binding competition and steric-hindrance with cis-regulatory factors at the site of tran-scription (dpp 30 and reaper 31,32 are both known to play a developmental role in wild-type eyes). Subtle increases in the expression of developmental genes induced through dCas9-VPR are known to have pronounced developmental phenotypes when expressed in Drosophila tissues 23 .…”