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This Article Full Text Full Text (PDF) [Supplemental Table] All Versions of this Article: 79/2/289    most recent biolreprod.107.067082v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Ma, W. Articles by Kistler, W. S. PubMed PubMed Citation Articles by Ma, W. Articles by Kistler, W. S. Agricola Articles by Ma, W. Articles by Kistler, W. S.

Expression Patterns of SP1 and SP3 During Mouse Spermatogenesis: SP1 Down-Regulation Correlates with Two Successive Promoter Changes and Translationally Compromised Transcripts¹

Department of Chemistry and Biochemistry, University of South Carolina, Columbia, South Carolina 29208

ABSTRACT

Because of their prominent roles in regulation of gene expression, it is important to understand how levels of Krüpple-like transcription factors SP1 and SP3 change in germ cells during spermatogenesis. Using immunological techniques, we found that both factors decreased sharply during meiosis. SP3 declined during the leptotene-to-pachytene transition, whereas SP1 fell somewhat later, as spermatocytes progressed beyond the early pachytene stage. SP3 reappeared for a period in round spermatids. For Sp1, the transition to the pachytene stage is accompanied by loss of the normal, 8.2-kb mRNA and appearance of a prevalent, 8.8-kb variant, which has not been well characterized. We have now shown that this pachytene-specific transcript contains a long, unspliced sequence from the first intron and that this sequence inhibits expression of a reporter, probably because of its many short open-reading frames. A second testis-specific Sp1 transcript in spermatids of 2.4 kb also has been reported previously. Like the 8.8-kb variant, it is compromised translationally. We have confirmed by Northern blotting that the 8.8-, 8.2-, and 2.4-kb variants account for the major testis Sp1 transcripts. Thus, the unexpected decline of SP1 protein in the face of continuing Sp1 transcription is explained, in large part, by poor translation of both novel testis transcripts. As part of this work, we also identified five additional, minor Sp1 cap sites by 5' rapid amplification of cDNA ends, including a trans-spliced RNA originating from the Glcci1 gene.

alternate promoter, alternative splicing, meiosis, mouse, spermatogenesis, SP1, SP3, testis, transcription factor

¹Supported by National Institutes of Health grant HD10793.

Correspondence: ²W. Stephen Kistler, Dept. of Chemistry & Biochemistry, University of South Carolina, Columbia, SC 29208. FAX: 803 777 9521; e-mail: wskistler{at}sc.edu