“…The SIN signal begins with the activity of the GTPase Spg1p and involves a regulatory GAP complex, several scaffolds and a linear cascade of three kinases (Cdc7p,Sid1p,and Sid2p), in order of their activation. Substrates of the Sid2p kinase are the phosphatase Clp1p/Flp1p (Mishra, Karagiannis, Sevugan, Singh, & Balasubramanian, 2005), the formin Cdc12p (Bohnert & Gould, 2012), the SIN scaffold Cdc11p (Feoktistova et al, 2012), the kinesin Klp2p (Mana-Capelli, McLean, Chen, Gould, & McCollum, 2012), the SAD kinase Cdr2p (Rincon et al, 2017), the anillin Mid1p (Willet, DeWitt, Beckley, Clifford, & Gould, 2019) and several others (Grallert, Connolly, Smith, Simanis, & Hagan, 2012;Gupta et al, 2013). Overexpression of Rho GTPase Rho1p, its GEFs Rgf1p and Rgf3p, as well as inactivation of Rho1p GAPs, partially rescues the lethality of sid2 mutants at a low restrictive temperature (Alcaide-Gavilan, Lahoz, Daga, & Jimenez, 2014;Jin, Zhou, Bimbo, Balasubramanian, & McCollum, 2006).…”