Relish plays a dynamic role in the niche to modulate Drosophila blood progenitor homeostasis in development and infection
Abstract
Immune challenges demand the gearing up of basal hematopoiesis to combat infection. Little is known about how during development, this switch is achieved to take care of the insult. Here, we show that the hematopoietic niche of the larval lymph gland of Drosophila senses immune challenge and reacts to it quickly through the nuclear factor-κB (NF-κB), Relish, a component of the immune deficiency (Imd) pathway. During development, Relish is triggered by ecdysone signaling in the hematopoietic niche to maintain the blood progenitors. Loss of Relish causes an alteration in the cytoskeletal architecture of the niche cells in a Jun Kinase dependent manner, resulting in the trapping of Hh implicated in progenitor maintenance. Notably, during infection, downregulation of Relish in the niche tilts the maintenance program towards precocious differentiation, thereby bolstering the cellular arm of the immune response.
Data availability
All data generated or analysed during this study are included in the manuscript and supporting files. Source data files have been provided for Figures 1- 7 and their respective supplemental figures.
Article and author information
Author details
Funding
DBT Wellcome Trust India Alliance (IA/S/17/503100)
- Lolitika Mandal
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Bruno Lemaître, École Polytechnique Fédérale de Lausanne, Switzerland
Version history
- Received: February 2, 2021
- Preprint posted: April 5, 2021 (view preprint)
- Accepted: July 14, 2021
- Accepted Manuscript published: July 22, 2021 (version 1)
- Version of Record published: August 13, 2021 (version 2)
Copyright
© 2021, Ramesh et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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