C. elegans germline stem cells become quiescent under starved conditions, and this quiescence maintains the stem cell state even in the absence of GLP-1/Notch signaling, which is otherwise essential for stem cell maintenance.
Fibroblast growth factor induces dephosphorylation and inactivation of the NPR2 guanylyl cyclase, thus decreasing cyclic GMP production in growth plate chondrocytes and contributing to FGF-dependent decreases in bone growth.
Structure-function analyses reveal the mechanistic underpinnings of inside-out transmembrane signaling that controls periplasmic proteolysis, and thereby biofilm formation, in bacteria and may be relevant in the context of other signaling proteins with similar control elements.
A newfound signaling enzyme that diverged from a protein family ubiquitous in bacteria provides mechanistic insights into how new signaling activity emerges to control distinct cellular function and physiology.
A cell-surface receptor called Gpr52 is able to lower the levels of the disease-causing protein mutant huntingtin and suppress its toxicity when knocked-down, making this receptor a promising drug target in Huntington's disease.