scholarly journals Family with Sequence Similarity 60A (FAM60A) Protein Is a Cell Cycle-fluctuating Regulator of the SIN3-HDAC1 Histone Deacetylase Complex

2012 ◽  
Vol 287 (39) ◽  
pp. 32346-32353 ◽  
Author(s):  
Ivan M. Muñoz ◽  
Thomas MacArtney ◽  
Luis Sanchez-Pulido ◽  
Chris P. Ponting ◽  
Sonia Rocha ◽  
...  
2007 ◽  
Vol 26 (3) ◽  
pp. 671-680 ◽  
Author(s):  
JoAnn M. Gensert ◽  
Oxana V. Baranova ◽  
David E. Weinstein ◽  
Rajiv R. Ratan

2004 ◽  
Vol 171 (4S) ◽  
pp. 93-94
Author(s):  
Hani Rashid ◽  
Susan Keay ◽  
Chen-Ou Zhang ◽  
Edward M. Messing ◽  
Jay Reeder

Genetics ◽  
2000 ◽  
Vol 154 (4) ◽  
pp. 1561-1576
Author(s):  
Neil Macpherson ◽  
Vivien Measday ◽  
Lynda Moore ◽  
Brenda Andrews

Abstract In Saccharomyces cerevisiae, the Swi6 protein is a component of two transcription factors, SBF and MBF, that promote expression of a large group of genes in the late G1 phase of the cell cycle. Although SBF is required for cell viability, SWI6 is not an essential gene. We performed a synthetic lethal screen to identify genes required for viability in the absence of SWI6 and identified 10 complementation groups of swi6-dependent lethal mutants, designated SLM1 through SLM10. We were most interested in mutants showing a cell cycle arrest phenotype; both slm7-1 swi6Δ and slm8-1 swi6Δ double mutants accumulated as large, unbudded cells with increased 1N DNA content and showed a temperature-sensitive growth arrest in the presence of Swi6. Analysis of the transcript levels of cell cycle-regulated genes in slm7-1 SWI6 mutant strains at the permissive temperature revealed defects in regulation of a subset of cyclin-encoding genes. Complementation and allelism tests showed that SLM7 is allelic with the TAF17 gene, which encodes a histone-like component of the general transcription factor TFIID and the SAGA histone acetyltransferase complex. Sequencing showed that the slm7-1 allele of TAF17 is predicted to encode a version of Taf17 that is truncated within a highly conserved region. The cell cycle and transcriptional defects caused by taf17slm7-1 are consistent with the role of TAFIIs as modulators of transcriptional activation and may reflect a role for TAF17 in regulating activation by SBF and MBF.


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