Terral, G. | Search bioRxiv

bioRxiv2020

A new mutant mouse model lacking mitochondrial-associated CB1 receptor

The idea that the effects of drugs largely depend on subcellular target location is emerging as a novel predictive factor of their beneficial or adverse outcomes. G protein-coupled type-1 cannabinoid receptors (CB1) are regulators of several brain functions as well as the main targets of cannabinoid-based medicines. Besides their classical location at plasma membranes, CB1 receptors are present at different locations within cells, including in association to mitochondrial membranes (mtCB1). Here we report the generation and characterization of a mutant mouse line, which lack mtCB1 receptors.

neuroscience↗

bioRxiv2020

An original structural fold underlies the multitask P1, a silencing suppressor encoded by the Rice yellow mottle virus

ABSTRACTThe Rice Yellow Mottle sobemovirus (RYMV) belongs to the most damaging pathogens devastating rice fields in Africa. P1, a key protein for RYMV, was reported as a potent RNAi suppressor counteracting RNA silencing in plant reporter systems. Here we describe the complete 3D structure and dynamics of P1. Its N-terminal region contains ZnF1, a structural CCCC-type zinc finger strongly affine to zinc and a prominent short helix, rendering this region poorly amenable to structural changes. P1 C-terminal region contains ZnF2, an atypical HCHC-type ZnF that does not belong to any existing class of Zn finger proteins. ZnF2 appeared much less affine to zinc and more sensitive to oxidizing environments than ZnF1, and may serve as a sensor of plant redox status. The structure helped us to identify key residues essential for RYMV infectivity and spread in rice tissues through their participation in P1 oligomerization and folding. Altogether, our results provide the first complete structure of an antiviral silencing suppressor encoded by a virus infecting rice and highlight P1 structural and dynamical properties that may serve RYMV functions to infect and invade its host plant.Competing Interest StatementThe authors have declared no competing interest.View Full Text

pathology↗