The Spg1p GTPase is an essential, dosage-dependent inducer of septum formation in Schizosaccharomyces pombe.

Abstract

The spgl gene (septum-promoting GTPase) was cloned as a multicopy suppressor of a dominant-negative mutant of the Cdc7p kinase. It encodes a small GTPase of the Ras superfamily, spgl is an essential gene. Null or heat-sensitive alleles do not make a division septum, but growth, S-phase, and mitosis continue in the absence of cell division, producing elongated, multinucleate cells. Increased expression of Spglp induces septum formation in G2, S-phase, and pre-Start Gl-arrested cells. This requires the activity of Cdc7p kinase, but not p34 cdc2. Increased expression of Cdc7p bypasses the requirement for Spglp. Spglp and Cdc7p can be coimmunoprecipitated from cell extracts, and interact in the two-hybrid system. These data indicate that Spglp is a key element in controlling the onset of septum formation in Schizosaccharomyces pombe, and that it acts through the Cdc7p kinase.

Localization of Fission Yeast Type II Myosin, Myo2, to the Cytokinetic Actin Ring Is Regulated by Phosphorylation of a C-Terminal Coiled-Coil Domain and Requires a Functional Septation Initiation Network

“…Any or all of the above are potential fission yeast myosin II heavy chain kinases. We have shown previously a genetic interaction between myo2 and cdc7 mutants (May et al, 1997;Mulvihill et al, 2000) and that the efficiency of septation driven by overexpression of Spg1, the GTPase activator of Cdc7 (Schmidt et al, 1997), or inactivation of Cdc16, one of the components of the Spg1 GTPase-activating protein (Furge et al, 1998), is substantially reduced in the mutant myo2-E1 (Mulvihill et al, 2000). In this report we show directly that the CAR is dependent for its integrity upon SIN function.…”

“…Mutations in Cdc7, Sid1, Sid2, and Spg1 abolish septation, whereas mutations in Cdc16 and Byr4 drive cells into cytokinesis and they become multiseptate (Minet et al, 1979;Fankhauser et al, 1993). A similar phenotype is seen when Cdc7 and Spg1 are overexproduced (Fankhauser and Simanis, 1994;Schmidt et al, 1997). The evidence that the SIN pathway also regulates Myo2 function includes a strong genetic interaction between a myo2 deletion strain and cdc7-24 (May et al, 1997) and the reduced efficiency of septation in myo2 mutants after overexpression of Spg1 or Cdc7, or the inactivation of Cdc16 (Mulvihill et al, 2000).…”

“…At the heart of this signal transduction pathway are three protein kinases, Cdc7, Sid1, and Sid2 (Fankhauser and Simanis, 1994;Sparks et al, 1999;Guertin et al, 2000) and their activating GTPase Spg1 (Schmidt et al, 1997). The timing of Spg1 activation is determined by a two-component GTPase-activating protein consisting of Cdc16 and Byr4 (Furge et al, 1998).…”

Centrosomes as signalling centres

“…In particular, Sid4 interacts with Plo1, a major activator of the SIN, whereas Cdc11 binds Spg1, thereby constitutively anchoring this GTPase to SPBs [56,57]. Spg1 drives the initiation of the SIN, and, when overexpressed, can trigger the onset of SIN signalling from any stage of the cell cycle [58]. In wild-type fission yeast, Spg1 is kept inactive during interphase by Byr4-Cdc16, and it is only activated upon entry into mitosis, when Byr4-Cdc16 dissociates from the SPBs [59,60].…”

Cytokinesis in Metazoa and Fungi

“…Direct activation of the SIN (Schmidt et al 1997), or its indirect activation by means of polo kinase Plo1 overexpression (Cullen et al 2000;Tanaka et al 2001), induces assembly of contractile rings and septa at various stages of the cell cycle. More downstream, overexpression of a truncated Cdc12 formin is also sufficient to induce ring assembly in interphase (Yonetani and Chang 2010).…”