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. 2008 Mar;178(3):1311–1325. doi: 10.1534/genetics.107.082511

Figure 10.—

Figure 10.—

A speculative model for sticky/citron kinase effects on gene expression. As previously shown (D'Avino et al. 2004), Rho is thought to activate while Rac inhibits sticky/citron kinase activity. We speculate that other (question mark) developmental and cellular cues may also impinge upon its activity. Active sticky/citron kinase can phosphorylate myosin to facilitate the completion of cytokinesis. Here we show that Ago1 activity may be dependent on sticky/citron kinase, although this may be indirect (dashed lines). Misexpression of genes in sticky/citron kinase mutants could be due to insufficient Ago1 protein activity, misregulation of RNAi processes, and/or misregulation of other factors (question mark) that modulate chromatin structure. Alterations in gene expression patterns can result from direct (solid arrows) or indirect (dashed arrows) regulation of one or more of these processes by sticky/citron kinase. Although it is not shown in this model, it is possible that cytokinesis can also be regulated by Ago1 and/or other RNAi components (Antar et al. 2005; Deshpande et al. 2005; Meyer et al. 2006). Furthermore, we speculate that sticky/citron kinase may function to link cell-cycle progression to epigenetic maintenance of heterochromatin.