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Kumar, J. P.

Publications and source records attributed to Kumar, J. P..

2 recordsLinked to original sources

Differential regulation of eye specification in Drosophila by Polycomb Group (PcG) epigenetic repressors

During metazoan development, chromatin plasticity and genetic regulation are tightly connected to establish proper tissue fate and patterning. Drosophila imaginal discs are excellent models to study these processes as both genetic and mechanical injury can redirect their fate during regeneration. Reducing expression of Polycomb (Pc) results in the ectopic activation of the wing selector gene vestigial (vg) which in turn interacts with its DNA-binding partner Scalloped (Sd) - this forces the eye to transform into a wing. Reductions of other PcG members alone does not phenocopy this transformation. However, knocking down Sex combs on midleg (Scm) or Scm-related gene containing four mbt domains (Sfmbt) alongside the Pax6 gene twin of eyeless (toy) enables the eye-to-wing transformation. Using high throughput sequencing we show that toy-Sfmbt and toy-Scm knockdowns alter expression of wing selector and Hox genes, respectively. These findings provide new insights into how the fate of the eye is specified. Author SummaryDistinct gene sets are differentially expressed in response to the knockdown of Polycomb Group (PcG) members suggesting multiple avenues may exist for the eye to be transformed into a wing.

developmental biology↗

Polycomb safeguards imaginal disc specification through control of the Vestigial-Scalloped complex

A fundamental goal of developmental biology is to understand how cell and tissue fates are specified. The imaginal discs of Drosophila are excellent model systems for addressing this paradigm as their fate can be redirected when discs regenerate after injury or when key selector genes are mis-regulated. Here, we show that when Polycomb expression is reduced, the wing selector gene vestigial is ectopically activated. This leads to the inappropriate formation of the Vestigial-Scalloped complex which forces the eye to transform into a wing. We further demonstrate that disrupting this complex does not simply block wing formation or restore eye development. Instead, immunohistochemistry and high throughput genomic analysis show that the eye-antennal disc unexpectedly undergoes hyperplastic growth with multiple domains being organized into other imaginal discs and tissues. These findings provide insight into the complex developmental landscape that tissues must navigate before adopting their final fate. Summary StatementHere we describe a novel mechanism by which Pc promotes an eye fate during normal development and how the eye is reprogrammed into a wing in its absence.

developmental biology↗