Vascular control of the Drosophila haematopoietic microenvironment by Slit/Robo signalling

Ismaël Morin-Poulard, Anurag Sharma, Isabelle Louradour, Nathalie Vanzo, Alain Vincent and Michèle Crozatier ()
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Ismaël Morin-Poulard: Centre de Biologie du Développement, UMR 5547 CNRS/Université Toulouse III and Fédération de Recherche de Biologie de Toulouse
Anurag Sharma: Centre de Biologie du Développement, UMR 5547 CNRS/Université Toulouse III and Fédération de Recherche de Biologie de Toulouse
Isabelle Louradour: Centre de Biologie du Développement, UMR 5547 CNRS/Université Toulouse III and Fédération de Recherche de Biologie de Toulouse
Nathalie Vanzo: Centre de Biologie du Développement, UMR 5547 CNRS/Université Toulouse III and Fédération de Recherche de Biologie de Toulouse
Alain Vincent: Centre de Biologie du Développement, UMR 5547 CNRS/Université Toulouse III and Fédération de Recherche de Biologie de Toulouse
Michèle Crozatier: Centre de Biologie du Développement, UMR 5547 CNRS/Université Toulouse III and Fédération de Recherche de Biologie de Toulouse

Nature Communications, 2016, vol. 7, issue 1, 1-12

Abstract: Abstract Self-renewal and differentiation of mammalian haematopoietic stem cells (HSCs) are controlled by a specialized microenvironment called ‘the niche’. In the bone marrow, HSCs receive signals from both the endosteal and vascular niches. The posterior signalling centre (PSC) of the larval Drosophila haematopoietic organ, the lymph gland, regulates blood cell differentiation under normal conditions and also plays a key role in controlling haematopoiesis under immune challenge. Here we report that the Drosophila vascular system also contributes to the lymph gland homoeostasis. Vascular cells produce Slit that activates Robo receptors in the PSC. Robo activation controls proliferation and clustering of PSC cells by regulating Myc, and small GTPase and DE-cadherin activity, respectively. These findings reveal that signals from the vascular system contribute to regulating the rate of blood cell differentiation via the regulation of PSC morphology.

Date: 2016
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11634

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DOI: 10.1038/ncomms11634

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