High impact information on SSD1

• A knockout of the SSD1 gene, which alters the composition and cell wall architecture of the yeast cell surface, causes both the clinical and plant isolates to be more virulent in the mouse model of infection [1].
• Here, we show that the cyt-4+ gene encodes a 120-kDa protein with significant similarity to the SSD1/SRK1 protein of Saccharomyces cerevisiae and the DIS3 protein of Schizosaccharomyces pombe, which have been implicated in protein phosphatase functions that regulate cell cycle and mitotic chromosome segregation [2].
• Assuming that the CYT-4 protein functions in a manner similar to the SSD1/SRK1 and DIS3 proteins, we infer that the mitochondrial RNA splicing and processing reactions defective in the cyt-4 mutants are regulated by protein phosphorylation and that the defects in the cyt-4 mutants result from failure to normally regulate this process [2].
• The different slk1 mutant defects are partially rescued by an extra copy of the SSD1/SRK1 gene [3].
• The Saccharomyces cerevisiae SRK1 gene, a suppressor of bcy1 and ins1, may be involved in protein phosphatase function [4].

Biological context of SSD1

• Deletion of TOR1 or TCO89 results in two specific and distinct phenotypes, (i) rapamycin-hypersensitivity and (ii) decreased cellular integrity, both of which correlate with the presence of SSD1-d, an allele of SSD1 previously associated with defects in cellular integrity [5].
• The SSD1 gene of Saccharomyces (S.) cerevisiae is a polymorphic gene involved in many aspects of the yeast cell growth (Sutton et al., 1991) [6].
• Deletion of SSD1-v or SSD1-d impeded sorting of the PIR proteins (osmotin-resistance factors) to the cell wall without affecting mRNA levels, indicating that SSD1 functions in post-transcriptional regulation of gene expression [7].
• Therefore SSD1 is an important regulator of fungal cell-wall biogenesis and composition, including the deposition of PIR proteins which block the action of plant antifungal PR-5 proteins [7].
• The SSD1 gene of Saccharomyces cerevisiae is a polymorphic locus that affects diverse cellular processes including cell integrity, cell cycle progression, and growth at high temperature [8].

Anatomical context of SSD1

• Saccharomyces cerevisiae MPT5 and SSD1 function in parallel pathways to promote cell wall integrity [9].

Associations of SSD1 with chemical compounds

• The ability of SRK1 to alleviate partially the defects caused by high levels of cyclic AMP-dependent protein kinase and the similarity of its encoded protein to dis3+ suggest that SRK1 may have a role in protein phosphatase function [4].

Regulatory relationships of SSD1

• The SSD1 protein is implicated in G1 control and has a region of similarity to the dis3 protein of Schizosaccharomyces pombe [10].

Other interactions of SSD1

• It was recently demonstrated that RAM genes are essential in strains containing functional SSD1 (SSD1-v), which encodes a protein of unknown function that binds the RAM Cbk1p kinase [11].
• Additionally, we describe a genetic interaction between RPT4 and the naturally polymorphic gene SSD1, which in wild-type form modifies the rpt4-145 phenotype such that cells arrest in G2 of the first cycle with complete bipolar spindles [12].
• The Saccharomyces cerevisiae SRK1 gene, when expressed on a low-copy shuttle vector, partially suppresses the phenotype associated with elevated levels of cyclic AMP-dependent protein kinase activity and suppresses the temperature-sensitive cell cycle arrest of the ins1 mutant [4].
• SRK1 is located on chromosome IV, 3 centimorgans from gcn2 [4].
• Deletions in SSD1 and PUF4, potential alternative regulators of cell integrity, also exhibit phenotypes [13].

References