How does RGA get recruited to cortical waves and what exactly is the nature of its relationship with F-actin? We aren't sure, but we plan to use immature frog oocytes and modeling to address these questions!

Modeling and experiments showed that Ect2 and RGA-3/4 are major drivers of this circuit, and just altering the relative levels of these two players produced a variety of cortical behaviors in an otherwise quiescent oocyte cortex!

We concluded that activated starfish oocytes and embryos and immature frog oocytes represent distinct phases on this excitability spectrum. Immature frog oocytes occupy the lower end while activated starfish oocytes and embryos occupy the higher end.

As the model ramped up the amount of RGA and entered the oscillatory domain, we saw an increase in amplitude and morphological features, and then a gradual decrease. In vivo experiments in oocytes closely paralleled these findings.

Modeling and experiments revealed two uniform states with no waves, separated by an oscillatory domain that supported a variety of cortical wave behavior. Bounding the oscillatory domain were regions of wave instability, characterized by pulsatile and spiral turbulence.

We used the immature frog oocyte system to look at some potential players in the excitability model: Anillin, myosin-2 and Dias 1-3. We showed the oocyte is a useful tool for studying these proteins further in the context of excitability.

Essentially, we took the wave dynamics seen in the embryonic furrow and induced them over the quasi-two-dimensional space of the oocyte cortex. This not only looks cool, but also allows us to collect high spatiotemporal data without complications present in embryos.

Light sheet imaging with @henryhetired and @spim revealed that these patterns were wide-spread and well-developed at merely 5hrs post-mRNA injection. This behavior was not seen with GAP-dead RGA or another cytokinetic GAP (p190RhoGAP).

To do this, we induced excitability in a cell type that does not naturally display it: the immature frog oocyte. We found that while Ect2 or RGA alone did not induce sustained excitability, co-expression of both led to high-amplitude, psychedelic waves that covered the cortex.