原创力文档sex reversal in zebrafish fancl mutants is caused by tp53-mediated germ cell apoptosis性逆转斑马鱼芳珂突变体是由tp53-mediated生殖细胞凋亡引起的.pdfVIP
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sex reversal in zebrafish fancl mutants is caused by tp53-mediated germ cell apoptosis性逆转斑马鱼芳珂突变体是由tp53-mediated生殖细胞凋亡引起的
Sex Reversal in Zebrafish fancl Mutants Is Caused by
Tp53-Mediated Germ Cell Apoptosis
´ ´1 ˜ 1¤ 1 1
Adriana Rodrıguez-Marı , Cristian Canestro , Ruth A. BreMiller , Alexandria Nguyen-Johnson ,
2,3 2,3 1
Kazuhide Asakawa , Koichi Kawakami , John H. Postlethwait *
1 Institute of Neuroscience, University of Oregon, Eugene, Oregon, United States of America, 2 Division of Molecular and Developmental Biology, National Institute of
Genetics, Mishima, Shizuoka, Japan, 3 Department of Genetics, The Graduate University for Advanced Studies (Sokendai), Mishima, Shizuoka, Japan
Abstract
The molecular genetic mechanisms of sex determination are not known for most vertebrates, including zebrafish. We
identified a mutation in the zebrafish fancl gene that causes homozygous mutants to develop as fertile males due to
female-to-male sex reversal. Fancl is a member of the Fanconi Anemia/BRCA DNA repair pathway. Experiments showed that
zebrafish fancl was expressed in developing germ cells in bipotential gonads at the critical time of sexual fate
determination. Caspase-3 immunoassays revealed increased germ cell apoptosis in fancl mutants that compromised oocyte
survival. In the absence of oocytes surviving through meiosis, somatic cells of mutant gonads did not maintain expression of
the ovary gene cyp19a1a and did not down-regulate expression of the early testis gene amh; consequently,
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