RhoD Inhibits RhoC-ROCK-Dependent Cell Contraction via PAK6

rho GTP-Binding Proteins 0301 basic medicine blebbing 610 TYROSINE KINASE Vaccinia virus cell contraction Article Cell Line 03 medical and health sciences Cell Movement Cell Line, Tumor RhoGTPase crosstalk Humans CORTICAL ACTIN IN-VIVO 11 Medical and Health Sciences TAIL FORMATION 0303 health sciences Tumor Science & Technology VACCINIA VIRUS-INFECTION F11L-MEDIATED INHIBITION ACTIN-BASED MOTILITY Cell Biology STRESS FIBERS RhoC 06 Biological Sciences RhoD NUCLEOTIDE EXCHANGE FACTOR Actins 3. Good health Pak6 p21-Activated Kinases rhoC GTP-Binding Protein PDZ-RHOGEF rhoA GTP-Binding Protein Life Sciences & Biomedicine Developmental Biology Signal Transduction
DOI: 10.1016/j.devcel.2017.04.010 Publication Date: 2017-05-08T16:32:35Z
ABSTRACT
RhoA-mediated regulation of myosin-II activity in the actin cortex controls the ability of cells to contract and bleb during a variety of cellular processes, including cell migration and division. Cell contraction and blebbing also frequently occur as part of the cytopathic effect seen during many different viral infections. We now demonstrate that the vaccinia virus protein F11, which localizes to the plasma membrane, is required for ROCK-mediated cell contraction from 2 hr post infection. Curiously, F11-induced cell contraction is dependent on RhoC and not RhoA signaling to ROCK. Moreover, RhoC-driven cell contraction depends on the upstream inhibition of RhoD signaling by F11. This inhibition prevents RhoD from regulating its downstream effector Pak6, alleviating the suppression of RhoC by the kinase. Our observations with vaccinia have now demonstrated that RhoD recruits Pak6 to the plasma membrane to antagonize RhoC signaling during cell contraction and blebbing.
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