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Originally published as Genetics Published Articles Ahead of Print on March 2, 2005.
Genetics, Vol. 170, 87-94, May 2005, Copyright © 2005
doi:10.1534/genetics.104.039214
Evidence That Spt10 and Spt21 of Saccharomyces cerevisiae Play Distinct Roles in Vivo and Functionally Interact With MCB-Binding Factor, SCB-Binding Factor and Snf1
David Hess1 and Fred Winston2
Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115
2 Corresponding author: Department of Genetics, Harvard Medical School, 77 Ave. Louis Pasteur, Boston, MA 02115.
E-mail: winston{at}genetics.med.harvard.edu
Mutations in SPT10 and SPT21 of Saccharomyces cerevisiae have been previously shown to cause two prominent mutant phenotypes: (1) defects in transcription of particular histone genes and (2) suppression of Ty and 
-insertion mutations (Spt– phenotype). The requirement for Spt10 and Spt21 for transcription of particular histone genes suggested that they may interact with two factors previously shown to be present at histone loci, SBF (Swi4 and Swi6) and MBF (Mbp1 and Swi6). Therefore, we have studied swi4
, mbp1, and swi6 mutants with respect to histone gene transcription and for interactions with spt10 and spt21. Our results suggest that MBF and SBF play only modest roles in activation of histone gene transcription. In addition, we were surprised to find that swi4, mbp1, and swi6 mutations suppress the spt21 Spt– phenotype, but not the spt21 defect in histone gene transcription. In contrast, both swi4 and mbp1 cause lethality when combined with spt10. To learn more about mutations that can suppress the spt21 Spt– phenotype, we performed a genetic screen and identified spt21 suppressors in seven additional genes. Three of these spt21 suppressors also cause lethality when combined with spt10. Analysis of one spt21 suppressor, reg1, led to the finding that hyperactivation of Snf1 kinase, as caused by reg1, suppresses the Spt– phenotype of spt21. Taken together, these genetic interactions suggest distinct roles for Spt21 and Spt10 in vivo that are sensitive to multiple perturbations in transcription networks.
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