Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Combined Automated Annotation using Multiple IEA Methods
Falcon deep research report for MIH1
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Summarises Kennedy et al. 2016 (PMID:26715668): purified Mih1 directly dephosphorylates Swe1-phosphorylated Cdc28-Clb2, and Ptp1 plus a PP2A-Rts1-dependent activity provide redundant Tyr19 dephosphorylation.
"Purified Mih1 removed Cdc28 Tyr19 phosphorylation directly."
Global analysis of protein localization in budding yeast.
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Genome-wide GFP-fusion localization collection in which Mih1 was scored in the cytoplasm and nucleus.
"a collection of yeast strains expressing full-length, chromosomally tagged green fluorescent protein fusion proteins"
Conservation of mitotic controls in fission and budding yeasts.
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MIH1 was identified as the budding-yeast structural and functional homolog of fission-yeast cdc25+, counteracting wee1+ kinase activity.
"The wee1+ activity is counteracted in S. cerevisiae by the gene product of MIH1, a newly identified gene capable of encoding a protein of MW 54,000, which is a structural and functional homolog of the cdc25+ mitotic inducer of fission yeast."
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wee1+ expression blocks mitotic initiation in cells lacking MIH1, placing Mih1 at the G2/M transition.
"Expression of wee1+ in a mih1- strain prevents the initiation of mitosis."
Swe1 and Mih1 regulate mitotic spindle dynamics in budding yeast via Bik1.
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The phosphorylation state of Mih1, controlled by Swe1 and Cdc5, is important for mitotic spindle elongation; Swe1 and Mih1 control Bik1 phosphorylation.
"Swe1 and the Polo-like kinase Cdc5 control the balance between phosphorylated and unphosphorylated forms of Mih1, which is, in turn, important for mitotic spindle elongation."
Properties of Saccharomyces cerevisiae wee1 and its differential regulation of p34CDC28 in response to G1 and G2 cyclins.
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The G2 delay of mih1 mutants is entirely dependent on SWE1, establishing Mih1 as the phosphatase opposing Swe1 on Cdc28.
"deletion of SWE1 did not alter the cell cycle but did eliminate the G2 delay observed in mih1- mutants"
Cdc28 tyrosine phosphorylation and the morphogenesis checkpoint in budding yeast.
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Nuclear-division timing in unbudded cells is exquisitely sensitive to SWE1 and MIH1 dosage, making the Swe1-Mih1 pair the output of the morphogenesis checkpoint.
"The timing of nuclear division in cells that cannot make a bud is exquisitely sensitive to the dosage of SWE1 and MIH1 genes, which control phosphorylation of Cdc28 at tyrosine 19."
A morphogenesis checkpoint monitors the actin cytoskeleton in yeast.
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MIH1 overexpression suppresses the lethality of SWE1 overexpression, demonstrating that Mih1 positively drives mitotic entry against Swe1.
"GAL1::MIH1 rescues the lethality of a GAL1::SWE1 strain grown on galactose media."
Septin-dependent assembly of a cell cycle-regulatory module in Saccharomyces cerevisiae.
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Loss of MIH1 converts the septin-mutant Swe1-dependent G2 delay into a permanent arrest, and hsl1 mih1 and hsl7 mih1 double mutants are inviable.
"deletion of MIH1 exacerbated the elongated-bud phenotype (Fig. 1 , panel 6), and these cells arrested permanently with a single nucleus"
Cdk1 regulates centrosome separation by restraining proteolysis of microtubule-associated proteins.
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Mih1 catalyses Cdc28 tyrosine 19 dephosphorylation, which is required for Cdc28 activation and SPB separation.
"cells unable to activate Cdc28 by tyrosine 19 dephosphorylation (Y19) catalyzed by Mih1 (homolog of Cdc25 phosphatase)"
Spatial regulation of Cdc55-PP2A by Zds1/Zds2 controls mitotic entry and mitotic exit in budding yeast.
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Mih1 removes the Swe1-dependent inhibitory phosphorylation of Cdc28 Tyr19 to promote mitotic entry, and is hyperphosphorylated in cdc55 and zds1 zds2 mutants.
"Mih1 phosphatase (Cdc25 homologue) removes this inhibitory phosphorylation to promote mitotic entry"
The Mck1 GSK-3 kinase inhibits the activity of Clb2-Cdk1 post-nuclear division.
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Mih1 antagonises Swe1-dependent Cdk1-Y19 phosphorylation but, unlike S. pombe cdc25, is not essential; it is hyperphosphorylated early in the cycle and dephosphorylated at mitotic entry.
"Mih1 is hyperphosphorylated early in the cell cycle and dephosphorylated as cells enter mitosis."
Budding yeast greatwall and endosulfines control activity and spatial regulation of PP2A(Cdc55) for timely mitotic progression.
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PP2A-Cdc55 dephosphorylates and activates Mih1, and the endosulfines Igo1/Igo2 are needed for timely Cdk1-Tyr19 and Mih1 dephosphorylation.
"PP2ACdc55 dephosphorylates and activates Mih1"
Polo-like kinase Cdc5 orchestrates Cdk1 regulation via Swe1 and Mih1 during meiotic prophase I exit.
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Meiosis I entry after recombination-checkpoint release depends on Cdc28-Tyr19 dephosphorylation governed by Swe1 versus Mih1; Cdc5 promotes Mih1 nuclear translocation.
"Cdc5 promotes Cdk1 activation by inducing Swe1 degradation and facilitating Mih1 nuclear translocation."
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Mih1 is cytoplasmic in meiotic prophase I and enters the nucleus at the prophase I to metaphase I transition.
"Microscopy studies revealed that, during meiotic prophase I, Mih1 was predominantly cytoplasmic and largely excluded from the nucleus. As cells transitioned from prophase I to metaphase I, Mih1 progressively accumulated in the nucleus, coinciding with SPB separation."
A CDC25 family protein phosphatase gates cargo recognition by the Vps26 retromer subunit.
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Mih1 directly dephosphorylates the Vps26 retromer subunit, and Vps26 phosphorylation state controls cargo binding and retromer-mediated sorting.
"Mih1 directly modulates the phosphorylation state of the Vps26 retromer subunit"
SGD gene description for MIH1 (yeast)