Genetic and molecular analyses reveal the decisive role of fatty acid oxidation (FAO) acting downstream to the ROS-JNK circuit essential for hemocyte progenitor differentiation in Drosophila..

Occluding-junctions form a permeability barrier around the hematopoietic niche in Drosophila that controls the production of immune cells in response to infection by shaping the signalling micro-environment produced by the niche.

Conditional deletion of TGFβ signaling results in tenocyte dedifferentiation in vivo demonstrating a key role for TGFβ signaling in the maintenance of the tendon cell fate.

Rab5 and Rab11 regulate hematopoietic homeostasis in Drosophila, and this process involves the JNK, Toll, and Ras/EGFR signaling pathways and autophagy.

Jumu is required for the proper differentiation of prohemocytes and the proliferation and location of PSC cells.

METTL3-mediated m6A modification maintains proper cell lineage specification during skin epithelium morphogenesis by coupling transcription and translation of key regulatory pathways.

Two niches contribute to the control of Drosophila blood cell homeostasis through their differential regulation of hematopoietic progenitors.

The timing and outcome of mammalian cell lineage decisions can be controlled by slow, stochastic events on individual regulatory gene loci.

Comprehensive developmental in situ analysis of the Drosophila lymph gland provides markers highlighting blood progenitor diversity and reveals that JAK-STAT signaling prevents posterior progenitor differentiation, promoting survival after immune challenge.

In the Drosophila hematopoietic microenvironment, a regulatory network involving Toll/NF-B, EGFR signaling and reactive oxygen species controls blood cell production in response to immune stress.