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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2008.02.033 Byline: Yi Ying Wang (a), Amanda Charlesworth (b)(c), Shannon M. Byrd (e), Robert Gregerson (f), Melanie C. MacNicol (b)(c), Angus M. MacNicol (a)(b)(d) Abstract: Cell cycle progression during oocyte maturation requires the strict temporal regulation of maternal mRNA translation. The intrinsic basis of this temporal control has not been fully elucidated but appears to involve distinct mRNA 3' UTR regulatory elements. In this study, we identify a novel translational control sequence (TCS) that exerts repression of target mRNAs in immature oocytes of the frog, Xenopus laevis, and can direct early cytoplasmic polyadenylation and translational activation during oocyte maturation. The TCS is functionally distinct from the previously characterized Musashi/polyadenylation response element (PRE) and the cytoplasmic polyadenylation element (CPE). We report that TCS elements exert translational repression in both the Wee1 mRNA 3' UTR and the pericentriolar material-1 (Pcm-1) mRNA 3' UTR in immature oocytes. During oocyte maturation, TCS function directs the early translational activation of the Pcm-1 mRNA. By contrast, we demonstrate that CPE sequences flanking the TCS elements in the Wee1 3' UTR suppress the ability of the TCS to direct early translational activation. Our results indicate that a functional hierarchy exists between these distinct 3' UTR regulatory elements to control the timing of maternal mRNA translational activation during oocyte maturation. Author Affiliation: (a) Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Slot 814, 4301 W. Markham St., Little Rock, AR 72205, USA (b) Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Slot 814, 4301 W. Markham St., Little Rock, AR 72205, USA (c) The Center for Translational Neuroscience, University of Arkansas for Medical Sciences, Slot 814, 4301 W. Markham St., Little Rock, AR 72205, USA (d) The Winthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences, Slot 814, 4301 W. Markham St., Little Rock, AR 72205, USA (e) Committee on Developmental Biology, The University of Chicago, Chicago, IL, USA (f) Science Division, Lyon College, Batesville, AR, USA Article History: Received 5 June 2007; Revised 14 February 2008; Accepted 15 February 2008

The second Adh2 gene of Petunia was cloned and analyzed using polymerase chain reaction. Nucleotide sequence, genetic mapping and northern analyses showed that the gene encodes ADH2. In a related study, the structures and expressions of Adh1 and Adh2 genes of Petunia were compared with those of the Adh genes of maize. The results showed similar mode of regulation for the pair of genes in both Petunia and maize.