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Biology of Reproduction 64, 507-517 (2001)
© 2001 Society for the Study of Reproduction, Inc.


Regular Article

TFIIA{alpha}/ß-Like Factor Is Encoded by a Germ Cell-Specific Gene Whose Expression Is Up-Regulated with Other General Transcription Factors During Spermatogenesis in the Mouse1

SangYoon Hana, Liping Zhoub, Ashok Upadhyayaa, Sang Hyun Leea, Keith L. Parkerb, and Jeff DeJong2,a

a The University of Texas at Dallas, Department of Molecular and Cell Biology, Richardson, Texas 75080 b The University of Texas Southwestern Medical Center, Departments of Internal Medicine and Pharmacology, Dallas, Texas 75235

ABSTRACT

TFIIA{alpha}/ß-like factor (ALF) is a testis-specific counterpart of the large subunit of human general transcription factor TFIIA. Northern analysis shows that ALF mRNA first appears in mouse testis at Postnatal Day 14. Similarly, expression of the general transcription factors TBP, TRF2, TFIIA{alpha}/ß, TFIIA{gamma}, and TFIIIB90 is also increased beginning at Postnatal Day 14, suggesting that there is a coordinated induction of many general transcription factors during male germ cell differentiation. Analysis of male germ cells separated by Staput sedimentation shows that ALF is present in pachytene spermatocytes and haploid spermatids. In addition, in situ hybridization experiments with adult mouse testis shows that ALF is present in haploid spermatids. Searches of the human genome sequence database using the basic local alignment search tool reveal that the ALF and TFIIA{alpha} (GTF2A1) genes are both composed of nine exons, whereas the TFIIA{gamma} (GTF2A2) gene is composed of five exons. Furthermore, nucleotide and amino acid comparisons among human and mouse ALF, TFIIA{alpha}/ß, and TFIIA{gamma} cDNA sequences show that ALF has diverged more rapidly than either TFIIA{alpha}/ß or TFIIA{gamma}. Finally, the ALF and SBLF (Stoned B-Like Factor) sequences present in the chimeric SALF cDNA are both present on human chromosome 2, and an analysis of the corresponding genes suggests a model for the formation of SALF.

FOOTNOTES

First decision: 31 May 2000.

1 This work was supported by grants from the American Cancer Society and the Welch Foundation (J.D.), and by NIH grant DK54480 (K.L.P.)

2 Correspondence: Jeff DeJong, The University of Texas at Dallas, Dept. of Molecular and Cell Biology, 2601 N. Floyd Rd., Richardson, TX 75080. FAX: 972 883 2409; dejong{at}utdallas.edu




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