Earlier studies have shown the PAR proteins (required for polarization of the embryo) and heterotrimeric G proteins (consisting of α, β and γ subunits) regulate spindle asymmetry in the early embryo. Mutation of two Gα subunits – GOA1 and GPA16 – resulted in symmetric cell division, even though polarity markers were properly localized, suggesting that G-protein signalling may be involved in coupling polarity signals to spindle position. However, relatively little is known about how GOA-1 or GPA-16 are regulated or how they might govern spindle asymmetry.
In this study, Gotta et al. start by demonstrating that inactivation of GPR-1 and GPR-2 results in a symmetric first division. However, they also found that polarity markers such as PAR-2 and PAR-3, which are important for spindle positioning, are correctly localized. This suggests the GPR-1/GPR-2 might function downstream of PAR-2 and PAR-3. Because PAR-2 and PAR-3 are known to regulate pulling forces at the spindle, the authors then assayed for spindle forces. Using inhibitory RNA strategies (RNAi) to block gpr-1/gpr-2 expression, they determined that the forces at both spindle poles in RNAi-treated embryos treated were weak when compared with wild-type embryos. They also found that in single-celled wild-type embryos, GPR-1/GPR-2 was enriched at the pole, where spindle forces are stronger. In addition, the asymmetric distribution of GPR-1/GPR-2 was found to be dependent on PAR-2 and PAR-3. These observations begin to provide a framework for understanding how PAR-2 and PAR-3 direct generation of asymmetric forces at the spindle poles.
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