Phosphorylation of Ind by MAP kinase enhances Ind-dependent transcriptional repression

Cade Moses, Aharon Helman, Ze'ev Paroush, Tonia Von Ohlen*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

The . Drosophila neuroectoderm is initially subdivided into three longitudinal domains that give rise to columns of neuroblasts. This subdivision is coordinately accomplished by the action of the signaling pathways, Dorsal and Epidermal Growth Factor Receptor (EGFR), in conjunction with the homeodomain proteins, Ventral nervous system defective, Intermediate neuroblasts defective (Ind) and Muscle Segment Homeobox. We previously demonstrated that Ind expression is activated in response to the EGFR pathway. Here we show that EGF signaling subsequently mediates the direct phosphorylation of Ind by MAP kinase, which enhances the capacity of Ind to repress target genes, such as . achaete. Specifically, we show that reduced EGF signaling results in diminished repression of . achaete in the intermediate column, despite the presence of high levels of Ind protein. We also demonstrate that ectopic activation of MAP kinase results in the lateral expansion of the Ind expression domain with a corresponding reduction in . achaete expression. This regulation is also dependent on the co-repressor, Dichaete. Our data indicate that EGF signaling, acting through MAP kinase, impinges on multiple aspects of Ind regulatory activity. While it has been often demonstrated that MAP kinase phosphorylation of transcriptional repressors attenuates their repressor activity, here we provide an example of phosphorylation enhancing repressor activity.

Original languageAmerican English
Pages (from-to)208-215
Number of pages8
JournalDevelopmental Biology
Volume360
Issue number1
DOIs
StatePublished - 1 Dec 2011

Bibliographical note

Funding Information:
We thank Dervla Mellerick (Science Word Doctor, LLC) for critical input, as well as writing and editing contributions. We also thank Amanda Simcox (Ohio State University), Jocelyn Mc Donald (Cleveland Clinic) and James Skeath (Washington University, St. Louis) for fly lines. This research was supported in part by a pilot award from the Provost's Office at Kansas State University as part of the Targeted Excellence in Arthropod Genomics to T.V.O. Support was also provided by the Israel Science Foundation (Center of Excellence 180/09 to Z. P.) and the Król Charitable Foundation (to Z. P.).

Keywords

  • Drosophila
  • Egfr signaling
  • Intermediate neuroblasts defective
  • Map kinase
  • Neuroectoderm

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