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Gene Review

MIG1  -  Mig1p

Saccharomyces cerevisiae S288c

Synonyms: CAT4, Regulatory protein CAT4, Regulatory protein MIG1, SSN1, TDS22, ...
 
 
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Disease relevance of MIG1

 

High impact information on MIG1

  • In addition to previously identified targets, Abf1, Rap1 and Mig1 bound to 107, 90 and 75 putative new target intergenic regions, respectively, many of which were upstream of previously uncharacterized open reading frames [3].
  • In addition, we show that the Cyc8-Tup1 complex functions both as a corepressor and an inhibitor of Mig1, a protein that binds to promoters of glucose-repressible genes [4].
  • One of the main roles of Snf1 is to relieve repression by the Mig1 complex, but it is also required for the operation of transcription factors such as Adr1 and possibly other factors that are still unidentified [5].
  • Genetic studies demonstrated that this binary response resulted from regulation of a second repressor, Gal80, whereas regulation of Mig1 by a distinct signaling pathway generated graded changes in GAL1 promoter activity [6].
  • Our studies demonstrate that a given promoter can adapt either binary or graded behavior, and identify the Mig1 and Gal80 genes as necessary for binary versus graded behavior of the Gal1 promoter [6].
 

Chemical compound and disease context of MIG1

 

Biological context of MIG1

 

Associations of MIG1 with chemical compounds

  • Mutations in SSN3 and SSN8 also act synergistically with a mutation of the MIG1 repressor protein to relieve glucose repression [11].
  • Binding of the MIG1 repressor to the glucose-repressible GAL1 and GAL4 promoters was analyzed in vivo by cyclobutane dimer footprinting in two yeast strains that show different glucose repression responses [12].
  • Evidence is presented indicating that, in addition to its role in the inactivation of Mig1p, Snf1p is required post-transcriptionally for the synthesis of maltose permease whose function is essential for maltose induction [13].
  • Mig1 and Hxk2 interacted in vivo in a yeast two-hybrid assay and in vitro in immunoprecipitation and glutathione S-transferase pull-down experiments [14].
  • We found that only three mutations within the GC box retain the ability to bind MIG1: G1 to C, C2 to T, and G5 to A [15].
 

Physical interactions of MIG1

  • Regions in the promoter of the yeast FBP1 gene implicated in catabolite repression may bind the product of the regulatory gene MIG1 [8].
  • Mutations of the two Mig1 binding sites in the SUC2 promoter resulted in loss of activation of SUC2 expression [16].
  • These results reveal new complexities in carbon response signaling, and may reflect the involvement of the Sip1 protein in the same complex as the Mig1 and Ssn6 proteins [17].
  • One molecular function of the Snf1 complex is deactivation by phosphorylation of the general glucose repressor Mig1 [18].
  • A disruption of MIG1 interacts synergistically with a disruption of GAL80, a gene involved in galactose induction [19].
  • These results allow postulating that the Hxk2 operates by interacting both with Mig1 and Snf1 to inhibit the Mig1 phosphorylation at serine 311 during high glucose grown [20].
 

Enzymatic interactions of MIG1

  • In immune complex assays of Snf1, coprecipitating Mig1 is phosphorylated in a Snf1-dependent reaction [21].
  • Finally, cells lacking the gamma subunit of the Snf1 kinase complex encoded by the SNF4 gene exhibited normal regulation of threonine 210 phosphorylation in response to glucose limitation but are unable to phosphorylate Mig1 efficiently [22].
 

Regulatory relationships of MIG1

  • The derepression defect of CAT8 in a cat1 mutant could be suppressed by a mutant Mig1p repressor protein [23].
  • Here we report that Hxk2 has a glucose-regulated nuclear localization and that Mig1, a transcriptional repressor responsible for glucose repression of many genes, is required to sequester Hxk2 into the nucleus [14].
  • Unexpectedly, we found that LexA-MIG1 activates transcription strongly in an ssn6 mutant and weakly in a tup1 mutant [24].
  • However, SUC2 expression is still about 13-fold repressed by glucose in a mig1 mutant [25].
  • The corresponding domain of the yeast Kluyveromyces lactis Mig1 conferred glucose-regulated Msn5-dependent protein export from the nucleus in S. cerevisiae [26].
 

Other interactions of MIG1

  • Its function was abolished in a mig1 mig2 double-deletion strain as well as in either ssn6 or tup1 single mutants [27].
  • A CAT8-lacZ promoter fusion revealed that the CAT8 gene itself is repressed by Cat4p (Mig1p) [28].
  • Analysis of the ENA1 promoter revealed a Mig1p-binding motif (-533 to -544) which was characterized as an upstream repressing sequence (URSMIG-ENA1) regulated by carbon source [27].
  • Expression of Mig1 could occur in the absence of Snf1 and was moderately sensitive to glucose [29].
  • We show that mig1 acts synergistically with ssn2 through ssn5, ssn7, and ssn8 to relieve glucose repression of SUC2 and to suppress the requirement for SNF1 [30].
 

Analytical, diagnostic and therapeutic context of MIG1

References

  1. Two homologous zinc finger genes identified by multicopy suppression in a SNF1 protein kinase mutant of Saccharomyces cerevisiae. Estruch, F., Carlson, M. Mol. Cell. Biol. (1993) [Pubmed]
  2. Lambda clone B22 contains a 7676 bp genomic fragment of Saccharomyces cerevisiae chromosome VII spanning the VAM7-SPM2 intergenic region and containing three novel transcribed open reading frames. Kail, M., Jüttner, E., Vaux, D. Yeast (1996) [Pubmed]
  3. Rapid analysis of the DNA-binding specificities of transcription factors with DNA microarrays. Mukherjee, S., Berger, M.F., Jona, G., Wang, X.S., Muzzey, D., Snyder, M., Young, R.A., Bulyk, M.L. Nat. Genet. (2004) [Pubmed]
  4. Distinct TPR motifs of Cyc8 are involved in recruiting the Cyc8-Tup1 corepressor complex to differentially regulated promoters. Tzamarias, D., Struhl, K. Genes Dev. (1995) [Pubmed]
  5. Yeast carbon catabolite repression. Gancedo, J.M. Microbiol. Mol. Biol. Rev. (1998) [Pubmed]
  6. Cell signaling can direct either binary or graded transcriptional responses. Biggar, S.R., Crabtree, G.R. EMBO J. (2001) [Pubmed]
  7. Negative control of the Mig1p repressor by Snf1p-dependent phosphorylation in the absence of glucose. Ostling, J., Ronne, H. Eur. J. Biochem. (1998) [Pubmed]
  8. Regions in the promoter of the yeast FBP1 gene implicated in catabolite repression may bind the product of the regulatory gene MIG1. Mercado, J.J., Vincent, O., Gancedo, J.M. FEBS Lett. (1991) [Pubmed]
  9. MIG1 overexpression causes flocculation in Saccharomyces cerevisiae. Shankar, C.S., Ramakrishnan, M.S., Umesh-Kumar, S. Microbiology (Reading, Engl.) (1996) [Pubmed]
  10. MIG1-dependent and MIG1-independent regulation of GAL gene expression in Saccharomyces cerevisiae: role of Imp2p. Alberti, A., Lodi, T., Ferrero, I., Donnini, C. Yeast (2003) [Pubmed]
  11. Cyclin-dependent protein kinase and cyclin homologs SSN3 and SSN8 contribute to transcriptional control in yeast. Kuchin, S., Yeghiayan, P., Carlson, M. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  12. Binding of the glucose-dependent Mig1p repressor to the GAL1 and GAL4 promoters in vivo: regulationby glucose and chromatin structure. Frolova, E., Johnston, M., Majors, J. Nucleic Acids Res. (1999) [Pubmed]
  13. Analysis of the mechanism by which glucose inhibits maltose induction of MAL gene expression in Saccharomyces. Hu, Z., Yue, Y., Jiang, H., Zhang, B., Sherwood, P.W., Michels, C.A. Genetics (2000) [Pubmed]
  14. The glucose-regulated nuclear localization of hexokinase 2 in Saccharomyces cerevisiae is Mig1-dependent. Ahuatzi, D., Herrero, P., de la Cera, T., Moreno, F. J. Biol. Chem. (2004) [Pubmed]
  15. Importance of a flanking AT-rich region in target site recognition by the GC box-binding zinc finger protein MIG1. Lundin, M., Nehlin, J.O., Ronne, H. Mol. Cell. Biol. (1994) [Pubmed]
  16. Multiple regulatory proteins mediate repression and activation by interaction with the yeast Mig1 binding site. Wu, J., Trumbly, R.J. Yeast (1998) [Pubmed]
  17. Genetic and carbon source regulation of phosphorylation of Sip1p, a Snf1p-associated protein involved in carbon response in Saccharomyces cerevisiae. Long, R.M., Hopper, J.E. Yeast (1995) [Pubmed]
  18. Transcriptional control of nonfermentative metabolism in the yeast Saccharomyces cerevisiae. Schüller, H.J. Curr. Genet. (2003) [Pubmed]
  19. Control of yeast GAL genes by MIG1 repressor: a transcriptional cascade in the glucose response. Nehlin, J.O., Carlberg, M., Ronne, H. EMBO J. (1991) [Pubmed]
  20. Hxk2 regulates the phosphorylation state of Mig1 and therefore its nucleocytoplasmic distribution. Ahuatzi, D., Riera, A., Peláez, R., Herrero, P., Moreno, F. J. Biol. Chem. (2007) [Pubmed]
  21. Snf1 protein kinase regulates phosphorylation of the Mig1 repressor in Saccharomyces cerevisiae. Treitel, M.A., Kuchin, S., Carlson, M. Mol. Cell. Biol. (1998) [Pubmed]
  22. Regulation of Snf1 kinase. Activation requires phosphorylation of threonine 210 by an upstream kinase as well as a distinct step mediated by the Snf4 subunit. McCartney, R.R., Schmidt, M.C. J. Biol. Chem. (2001) [Pubmed]
  23. Dual influence of the yeast Cat1p (Snf1p) protein kinase on carbon source-dependent transcriptional activation of gluconeogenic genes by the regulatory gene CAT8. Rahner, A., Schöler, A., Martens, E., Gollwitzer, B., Schüller, H.J. Nucleic Acids Res. (1996) [Pubmed]
  24. Repression by SSN6-TUP1 is directed by MIG1, a repressor/activator protein. Treitel, M.A., Carlson, M. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  25. Two zinc-finger-containing repressors are responsible for glucose repression of SUC2 expression. Lutfiyya, L.L., Johnston, M. Mol. Cell. Biol. (1996) [Pubmed]
  26. The nuclear exportin Msn5 is required for nuclear export of the Mig1 glucose repressor of Saccharomyces cerevisiae. DeVit, M.J., Johnston, M. Curr. Biol. (1999) [Pubmed]
  27. Repressors and upstream repressing sequences of the stress-regulated ENA1 gene in Saccharomyces cerevisiae: bZIP protein Sko1p confers HOG-dependent osmotic regulation. Proft, M., Serrano, R. Mol. Cell. Biol. (1999) [Pubmed]
  28. CAT8, a new zinc cluster-encoding gene necessary for derepression of gluconeogenic enzymes in the yeast Saccharomyces cerevisiae. Hedges, D., Proft, M., Entian, K.D. Mol. Cell. Biol. (1995) [Pubmed]
  29. Regulatory elements in the FBP1 promoter respond differently to glucose-dependent signals in Saccharomyces cerevisiae. Zaragoza, O., Vincent, O., Gancedo, J.M. Biochem. J. (2001) [Pubmed]
  30. Synergistic release from glucose repression by mig1 and ssn mutations in Saccharomyces cerevisiae. Vallier, L.G., Carlson, M. Genetics (1994) [Pubmed]
  31. Glucose sensing through the Hxk2-dependent signalling pathway. Moreno, F., Ahuatzi, D., Riera, A., Palomino, C.A., Herrero, P. Biochem. Soc. Trans. (2005) [Pubmed]
  32. Isolation and sequence of the MIG1 homologue from the yeast Candida utilis. Delfin, J., Perdomo, W., García, B., Menendez, J. Yeast (2001) [Pubmed]
  33. In vitro characterization of the Mig1 repressor from Saccharomyces cerevisiae reveals evidence for monomeric and higher molecular weight forms. Needham, P.G., Trumbly, R.J. Yeast (2006) [Pubmed]
  34. Mutations in GCR1 affect SUC2 gene expression in Saccharomyces cerevisiae. Türkel, S., Turgut, T., López, M.C., Uemura, H., Baker, H.V. Mol. Genet. Genomics (2003) [Pubmed]
 
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