Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Systematic identification of pathways that couple cell growth and division in yeast.
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Genome-wide cell-size profiling of the yeast deletion collection identified Whi5 as one of the five most potent regulators of critical cell size at Start.
"govern critical cell size at Start, the most potent of which were Sfp1, Sch9,"
Global analysis of protein localization in budding yeast.
Cln3 activates G1-specific transcription via phosphorylation of the SBF bound repressor Whi5.
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Whi5 is a stably bound component of SBF but not MBF, associates with G1-specific promoters via SBF in early G1 and dissociates upon Cln3/CDK-dependent phosphorylation.
"Whi5 was identified as a stably bound component of SBF but not MBF."
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whi5 inactivation bypasses the requirement for Cln3 for both G1/S transcription and cell-cycle initiation.
"Whi5 inactivation bypasses the requirement for Cln3 both for transcriptional activation and cell cycle initiation."
CDK activity antagonizes Whi5, an inhibitor of G1/S transcription in yeast.
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Whi5 inhibits G1/S transcription, is recruited to promoters via SBF/MBF, and is released and exported from the nucleus by CDK phosphorylation in late G1.
"In late G1 phase, CDK-dependent phosphorylation dissociates Whi5 from SBF and drives Whi5 out of the nucleus."
Systematic identification of cell cycle-dependent yeast nucleocytoplasmic shuttling proteins by prediction of composite motifs.
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Whi5 nuclear export is Msn5-dependent and Crm1-independent; Whi5 is constitutively nuclear in msn5 cells.
"Yen1, Psy4, Pds1, and Whi5 were constitutively localized to the nucleus in an msn5 Δ mutant, but not by treatment with leptomycin B (LMB), a Crm1 inhibitor"
The E2F functional analogue SBF recruits the Rpd3(L) HDAC, via Whi5 and Stb1, and the FACT chromatin reorganizer, to yeast G1 cyclin promoters.
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Whi5 and Stb1 are the redundant intermediaries through which SBF recruits the Rpd3(L) HDAC to CLN1/CLN2 promoters; Whi5 does not bind MBF.
"Rpd3(L) is recruited to SBF genes by both Stb1 and Whi5, and Rpd3(L) binding is only lost in the stb1 whi5 double mutant."
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In this strain background a whi5 single mutant shows nearly normal CLN1/CLN2 RNA, reflecting redundancy with Stb1.
"However, RNA measurements show nearly normal expression of CLN1 and CLN2 in whi5 mutants"
Dual regulation by pairs of cyclin-dependent protein kinases and histone deacetylases controls G1 transcription in budding yeast.
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Whi5 is a physiological substrate of Pcl9-Pho85 as well as Cln3-Cdc28; the G1 delay of cln3 pho85 cells is Whi5-dependent, and Whi5 represses partly through the HDACs Hos3 and Rpd3.
"The G1 delay phenotype associated with a cln3Δ pho85Δ strain is dependent on WHI5."
Recruitment of Cln3 cyclin to promoters controls cell cycle entry via histone deacetylase and other targets.
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Whi5 is an important but not the sole target of Cln3 at SBF promoters.
"Although Whi5 is clearly an important target of Cln3, and an important regulator of SBF, it may not be the only target."
The yeast Ess1 prolyl isomerase controls Swi6 and Whi5 nuclear localization.
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Whi5-GFP fails to accumulate in the nucleus in ess1H164R cells; Ess1 binds the phosphorylated Ser-Pro motifs of the Whi5 NLS/NES in vitro.
"In ess1H164R mutant cells, the fusion protein failed to localize to the nucleus and cytoplasmic staining was readily apparent"
Dilution of the cell cycle inhibitor Whi5 controls budding-yeast cell size.
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Whi5 is stable, synthesized in S/G2/M at a size-independent rate, and diluted by growth in G1; its concentration, not cell size per se, sets the rate of passage through Start.
"In this model, cell growth dilutes the cell cycle inhibitor Whi5 to drive progression through the cell cycle, whereas Cln3 concentration remains constant."
Omic AI reveals new autophagy regulators from the Atg1 interactome in Saccharomyces cerevisiae.
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whi5 deletion attenuates GFP-Atg8 processing under nitrogen starvation; Whi5 co-immunoprecipitates with Atg1 and is phosphorylated by Atg1 in vitro.
"Using the GFP-Atg8 immunoblotting assay, we found that the cleavage of GFP-Atg8 was significantly attenuated in yeast cells with deletion of WHI5 compared to WT cells"
WHI5 deep research (falcon literature synthesis)