A newly described isolate of the behavior-manipulating fly pathogen Entomophthora muscae that naturally infects fruit flies can be cultured in the lab, enabling molecular investigation of how microbes induce behavior changes in animal hosts.

Bacterial location quantifications highlights how Drosophila melanogaster larvae discriminate bacteria to isolate and later eliminate pathogens in the anterior midgut through coordinated mechanisms involving reactive oxygen species (ROS) and antimicrobial peptides (AMPs).

In C. elegans, neuronic TRPA-1 senses bacterial accumulation by detecting indole production to up-regulate lysozyme genes via FOXO/DAF-16 in the intestine, thereby delaying microbial dysbiosis.

The universal bacteria cell wall component peptidoglycan impacts the egg-laying behavior of infected Drosophila females by directly modulating the activity of few brain octopaminergic neurons.

A signaling pathway involving PGAM5, ASK1 and JNK induces persistent FoxO activation, chaperone expression and lifespan extension following developmental mitochondrial stress, which can be blocked by mTOR signaling through GCN-2.

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.

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.

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.