Biology subjects

Grenet, S.

Publications and source records attributed to Grenet, S..

3 recordsLinked to original sources

bioRxiv2026

Feedback between PI4P signaling and ER-PM contact sites orchestrates polarized root hair growth

Eukaryotic cells are composed of different organelles that communicate with one another through direct contacts, which are necessary for a host of cellular reactions and for responding to different developmental and environmental changes. Plasma membrane (PM) forms extensive contacts with the endoplasmic reticulum (ER) at specific sites named ER-PM contact sites. These contacts play crucial functions in lipid homeostasis, Ca2+ regulation and signaling in all eukaryotes. However, the mechanisms by which plant ER-PM contact site proteins tether to the PM, as well as the dynamics of these contact sites, remain poorly understood. Here, we investigate the importance of phosphoinositides in the establishment and dynamics of ER-PM contact site proteins in plants. We found that phosphatidylinositol-4-phosphate (PI4P), rather than phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), is required for the association of ER-PM contact site proteins with the PM. Furthermore, we identified a PI4P phosphatase, SUPPRESSOR-OF-ACTIN7 (SAC7), that associates with the ER-PM contact site protein SYNAPTOTAGMIN1 (SYT1) and regulates its dynamic association with the PM. In particular, we found that in growing root hairs, a highly polarized cell type, SAC7 removes SYT1-containing contact sites at the growing tip. Consistently, optogenetic induction of ER-PM tethering reduced root hair elongation within minutes of blue light induction. Altogether, we propose a link between SAC7-mediated regulation of PI4P, dynamic ER-PM contact site establishment and polarized cell growth in plants.

Plant Biology↗

bioRxiv2025

CSF1R regulates monocyte subset differentiation and intracellular metabolism.

Monocytes are key circulating effectors of vascular homeostasis, innate immunity and inflammation. Following their generation in mouse bone marrow, classical (Ly6Chigh) monocytes are mobilized into the blood circulation where they mature into non-classical (Ly6Clow) patrolling monocytes or are recruited into peripheral tissues where they differentiate into tissue resident or inflammatory macrophages. Monocytes and macrophages express CSF1R (CD115), the receptor for lineage-specific growth factors CSF1 and IL34. Here, we report that acute CSF1R blockade or genetic deletion negatively interferes with monocyte intracellular metabolism and reduces blood Ly6Clow monocytes in part by blunting differentiation of Ly6Chigh monocytes. Based upon lineage-specific deletion of GFPT1 (Glutamine-Fructose-6-Phosphate Transaminase 1), the hexosamine biosynthetic pathway (HBP) is identified as a novel regulator of CSF1R expression and monocyte subset diversity. Our findings provide new insights into the link between CSF1R signaling, metabolic regulation, and monocyte survival and differentiation.

immunology↗

bioRxiv2024

Autophagy acts as a brake on obesity-related fibrosis by controlling purine nucleoside signalling

A hallmark of obesity is a pathological expansion of white adipose tissue (WAT), accompanied by marked tissue dysfunction and fibrosis. Autophagy promotes adipocyte differentiation and lipid homeostasis, but its role in obese adipocytes and adipose tissue dysfunction remains incompletely understood. Here, we demonstrate that autophagy is a key tissue-specific regulator of WAT remodelling in diet-induced obesity. Importantly, loss of adipocyte autophagy substantially exacerbates pericellular fibrosis in visceral WAT. Change in WAT architecture correlates with increased infiltration of macrophages with tissue-reparative, fibrotic features. We uncover that autophagy regulates purine nucleoside metabolism in obese adipocytes, preventing excessive release of the purine catabolites xanthine and hypoxanthine. Purines signal cell-extrinsically for fibrosis by driving macrophage polarisation towards a tissue reparative phenotype. Our findings reveal a novel role for adipocyte autophagy in regulating tissue purine nucleoside metabolism, thereby limiting obesity-associated fibrosis and maintaining the functional integrity of visceral WAT. Purine signals may serve as a critical balance checkpoint and therapeutic target in fibrotic diseases.

cell biology↗