Disease relevance of NOT5

• We implicate C. albicans NOT5 in the pathogenesis of disseminated candidiasis (DC) induced by intravenous infection among neutropenic and nonimmunosuppressed mice, as well as in that of OPC in mice immunosuppressed with corticosteroids [1].

High impact information on NOT5

• Overexpression of C-terminally truncated yTAF1 is toxic in not4 or not5 mutants, whereas overexpression of full-length yTAF1 suppresses not4 [2].
• In contrast, the not2-4 allele destabilized the CCR4-NOT complex to a lesser extent and had no effect on NOT5 association with NOT2 [3].
• The essential C-terminal domain of Not1p can associate with Not5p, and both proteins are present in 1.2 and 2 MDa complexes in the absence of the N-terminal Not1p domain [4].
• The growth defect of a not5 mutant can be suppressed by a mot1 mutant [5].
• These findings suggest that the role of NOT5 in virulence depends on the specific in vivo environment and is influenced by diverse factors such as tissue site, portal of entry, and the status of host defenses [1].

Anatomical context of NOT5

• NOT5 is necessary for normal adherence to colonic and cervical epithelial cells in vitro, demonstrating that such assays cannot fully replicate disease processes in vivo [1].

Physical interactions of NOT5

• Thirdly, NOT5 interacts with NOT1 and NOT3 in the two-hybrid assay [6].

Regulatory relationships of NOT5

• First, overexpression of NOT3 or NOT4 suppresses mutations in NOT5 [6].

Other interactions of NOT5

• Secondly, mutations in NOT4 are synthetically lethal with mutations in NOT5 [6].
• NOT5 was subsequently shown to associate with TBP and TAFs and this association was dependent on the integrity of TFIID [7].

References