A complex of LIN-5 and GPR proteins regulates G protein signaling and spindle function inC. elegans

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Abstract
TheCaenorhabditis eleganscoiled-coil protein LIN-5 mediates several processes in cell division that depend on spindle forces, including alignment and segregation of chromosomes and positioning of the spindle. Here, we describe two closely related proteins, GPR-1 and GPR-2 (G proteinregulator), which associate with LIN-5 in vivo and in vitro and depend on LIN-5 for localization to the spindle and cell cortex. GPR-1/GPR-2 contain a GoLoco/GPR motif that mediates interaction with GDP-bound Gαi/o. Inactivation oflin-5,gpr-1/gpr-2, or the Gαi/ogenesgoa-1andgpa-16all cause highly similar chromosome segregation and spindle positioning defects, indicating a positive role for the LIN-5 and GPR proteins in G protein signaling. Thelin-5andgpr-1/gpr-2genes appear to act downstream of theparpolarity genes in the one- and two-cell stages and downstream of the tyrosine kinase-related genesmes-1andsrc-1at the four-cell stage. Together, these results indicate that GPR-1/GPR-2 in association with LIN-5 activate G protein signaling to affect spindle force. Polarity determinants may regulate LIN-5/GPR/Gα locally to create the asymmetric forces that drive spindle movement. Results inC. elegansand other species are consistent with a novel model for receptor-independent activation of Gαi/osignaling.