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Molecular and Cellular Biology, July 2006, p. 5120-5130, Vol. 26, No. 13
0270-7306/06/$08.00+0     doi:10.1128/MCB.01913-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Sbp1p Affects Translational Repression and Decapping in Saccharomyces cerevisiae

Scott P. Segal, Travis Dunckley,{dagger} and Roy Parker*

Department of Molecular Cellular Biology and Howard Hughes Medical Institute, University of Arizona, Tucson, Arizona 85721

Received 30 September 2005/ Returned for modification 31 October 2005/ Accepted 31 March 2006

The relationship between translation and mRNA turnover is critical to the regulation of gene expression. One major pathway for mRNA turnover occurs by deadenylation, which leads to decapping and subsequent 5'-to-3' degradation of the body of the mRNA. Prior to mRNA decapping, a transcript exits translation and enters P bodies to become a potential decapping substrate. To understand the transition from translation to decapping, it is important to identify the factors involved in this process. In this work, we identify Sbp1p (formerly known as Ssb1p), an abundant RNA binding protein, as a high-copy-number suppressor of a conditional allele in the decapping enzyme. Sbp1p overexpression restores normal decay rates in decapping-defective strains and increases P-body size and number. In addition, Sbp1p promotes translational repression of mRNA during glucose deprivation. Moreover, P-body formation is reduced in strains lacking Sbp1p. Sbp1p acts in conjunction with Dhh1p, as it is required for translational repression and P-body formation in pat1{Delta} strains under these conditions. These results identify Sbp1p as a new protein that functions in the transition of mRNAs from translation to an mRNP complex destined for decapping.

* Corresponding author. Mailing address: Department of Molecular Cellular Biology and Howard Hughes Medical Institute, University of Arizona, 1007 E. Lowell St., Tucson, AZ 85721. Phone: (520) 621-9347. Fax: (520) 621-4524. E-mail: rrparker{at}u.arizona.edu.

{dagger} Present address: Translational Genomics Research Institute, Neurogenomic Division, Phoenix, AZ 85004.

Molecular and Cellular Biology, July 2006, p. 5120-5130, Vol. 26, No. 13
0270-7306/06/$08.00+0     doi:10.1128/MCB.01913-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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