Sexual dimorphisms drive oocyte and spermatocyte development in zebrafish

Title Sexual dimorphisms drive oocyte and spermatocyte development in zebrafish
Lecturer Dr. Sean Burgess( Department of Molecular and Cellular Biology, University of California, Davis)
Language English
Date&Time 12/03/2015 (Thu) 13:30~14:30
Venue Large Seminar Room 
Detail Aneuploidy is the leading cause of birth defects and spontaneous abortions in humans.¹ The majority of these aneuploidies are maternally derived, and most of the clinically relevant cases of aneuploidy arise from segregation errors in meiosis I.² In our study we use the zebrafish, Danio rerio, to determine which meiotic processes may lead to a higher rate of aneuploidy production in the female than in the male. Using TALENs, we have generated two mutants with meiotic defects: spo11 and rad21l1. Spo11 is a meiotic protein that generates programmed double strand breaks that facilitate the formation of crossovers, and Rad21l1 is a meiosis specific cohesin subunit found only in vertebrates. We have shown that both spo11 and rad21l1 mutants have sexually dimorphic phenotypes. While spo11 males are sterile, spo11 females are able to produce offspring; however, most of these offspring are likely aneuploid and die before five days post fertilization. The rad21l1 mutants, on the other hand, have a defect in maintaining the female phenotype with over 97% of homozygotes developing into males, which appear to be fully fertile. Interestingly, in rad21l1/tp53 double mutants, the defect in maintaining femaleness is rescued but most of the double mutant females’ offspring are deformed. We have also observed telomere clustering in both males and females and have analyzed the loading of two components of the synaptonemal complex, Scp3 and Scp1, in males. Our preliminary data with Scp3 and Scp1 loading support that synapsis formation in the zebrafish initiates near the telomere ends, as has previously been shown by Saito et al., 2014.³ Furthermore, we found that γH2AX signal co-localizes with the telomere signal in male zygotene stage which suggests that the double strand breaks occur near the telomere ends, as is support by previous data with Mlh1 foci.4 We show that neither Scp3 loading nor the clustering of telomeres into bouquet formation is affected by the spo11 or the rad21l1 mutation in males. However, a normal pachytene stage has not yet been found in the spo11 mutants. In rad21l1 mutants, although the pachytene stage appears similar to wild type, we have seen some loading of Sycp1 in unpaired regions in the mutants but not in wild type.
Contact 原核生物分子遺伝学
真木 壽治 (

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