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Genetics, Vol. 170, 87-94, May 2005, Copyright © 2005
doi:10.1534/genetics.104.039214
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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
-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. This article has been cited by other articles:
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