Science 313:108 (2006/07)
David Pellman @ DFCI
In this paper, authors provided a possible link between Cdc5, the Polo-like kinase in yeast, and Rho1, the critical regulator in cytokinesis contractile ring construction. Authors stated “we found that budding yeast Polo-like kinase Cdc5 controls the targeting and activation of Rho1 (RhoA) at the division site via Rho1 guanine nucleotide exchange factors. This role of Cdc5 (Polo-like kinase) in regulating Rho1 is likely to be relevant to cytokinesis and asymmetric cell division in other organisms.
Authors specifically screened GEFs in yeast genome and found several candidates which interact with Cdc5. Functional assay showed at least Tus1 and Rom2 interacts with Cdc5 by a mechanism similar to that other known Polo substrates, that is, PBD binding to the pilot phosphorylation site on substrates. Authors also showed the Cdc5 phosphorylation targets Tus1 to the division sites. However, authors didn’t address much on the part between GEF Tus1 and Rho1, or the data is not solid / convincing enough for the title of this paper. How GEFs bring Rho1 to the division site? A live imaging experiment to clarify the spatial and temporal relationship between Cdc5, GEFs, and Rho1 will be great for addressing this issue.
At the end, authors referenced that RhoA GEF Ect2 is a substrate for Plk1 in vitro. So the similar task should be done in mammalian systems to make the story more complete.
The selected pictures in figures are crappy too. Since usually pictures shown in figures are the best pictures the authors have, it is very difficult to make conclusions based on those pictures if they are the best ones.
It is disappointing that the work between GEFs and Rho1, and at least trying other organisms are not been well done. It should not be a Science paper. The main reason it got accepted might be the novelty of Polo regulating Rho activity, and very likely because David Pellman is a pushy man too.
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