Project description:Hormad1 encodes a protein that contains a HORMA domain, and unlike Mad2, Hormad1 expression is germ cell specific. We discovered that both male and female are infertile, and HORMAD1 has important function in synaptonemal complex formation, sex chromosome inactivation during spermatogenesis and chromosome segregation in meiosis.
Project description:Meiosis creates genetic diversity by recombination and segregation of chromosomes. The synaptonemal complex assembles during meiotic prophase I and assists faithful exchanges between homologous chromosomes, but how its assembly/disassembly is regulated remains to be understood. Here we report how two major post-translational modifications, phosphorylation and ubiquitination, co-operate to promote synaptonemal complex assembly. We found that the ubiquitin ligase complex SCF is important for assembly and maintenance of the synaptonemal complex in Drosophila female meiosis. This function of SCF is mediated by two substrate-recognising F-box proteins, Slmb/βTrcp and Fbxo42. SCF-Fbxo42 downregulates the phosphatase subunit PP2A-B56, which is important for synaptonemal complex assembly and maintenance.
Project description:In our study, differential male nucleus events and development behaviors were revealed from the fertilized eggs in response to the sperm from males of genotypic sex determination (GSD) and temperature-dependent sex determination (TSD) in gibel carp. When the eggs of maternal fish were fertilized by the sperm from males of GSD, the fertilized egg encountered similar sexual reproduction events and behaviors. However, when the eggs of maternal fish were fertilized by the sperm from males of TSD, a typical process of gynogenesis was observed. To reveal the underlying molecular mechanism of differential sperm nucleus development behaviors in the fertilized eggs, iTRAQ-based quantitative semen proteomics were performed on three semen samples from three males of GSD and three semen samples from three males of TSD respectively.
Project description:Human eggs were fertilized with sperm carrying a homozygous mutation in the EYS gene at rs758109813 and treated with a Cas9 RNP targeting this mutation at either fertilization or at the 2-cell stage. The purpose of this analysis was to determine loss of heterozygosity due to CRISPR-induced chromosomal changes. We find that However, in half of the embryos, the break remains unrepaired throughout the first cell cycle, resulting in both segmental, as well as whole chromosome loss. These embryos appear as corrected non-mosaic wild type embryos in an on-target sequence analysis, but are not viable. These results show a surprising tolerance of the human embryo for mitotic entry with unrepaired DNA double strand breaks, and suggest that pericentromeric cleavage by Cas9 may enable the allele-specific removal of chromosomes in trisomic embryos.
Project description:We performed ATAC-seq in mouse sperms and fertilized eggs with wild-type or P1 mutation (phosphorylation sites by SRPK1) to capture early genome reprogramming events ~5 hours post insemination. Surprisingly, we detected broadly distributed ATAC-seq reads across the mouse genome to paternal and maternal gametes formed with wild-type and single mutant sperm, and in contrast, we saw individual peaks with zygotes formed with the double mutant sperm. After assigning to paternal and maternal genomes, we found that the reads assignable to paternal genome was decreased with single and double mutants, compare with wild-type. Furthermore, we found the paternal genome in eggs fertilized with the double mutant sperm essentially retained all sperm-specific ATAC-seq peaks, which were also overlapped with the published H3.3 ChIP-seq signals on wild-type sperm, mostly corresponding to TSSs. Strikingly, the ATAC-seq signals on the maternal genome from eggs fertilized with the double mutant P1 sperm were literally identical to those in MII oocyte. Based on these data, we draw two important conclusions: (i) dramatic chromatin remodeling takes place in a highly coordinated fashion in both paternal and maternal pronuclei before they merge, and (ii) SRPK1-catalyzed protamine phosphorylation initiates such synchronized genome reprogramming in both gametes.
Project description:Using a tiled whole-genome microarray, we found that 58.2% of Tribolium castaneum genes are maternally loaded into eggs. Comparison of known Drosophila melanogaster maternal genes to our results showed widespread conservation of maternal function with T. castaneum. We also found many T. castaneum genes with previously identified gender or tissue specific expression were also maternally loaded into eggs. The microarray design also allowed the detection of 2315 and 4060 novel transcriptionally active regions greater in length than 100 bp in unfertilized and fertilized T. castaneum eggs, respectively. The primary objective of this study was to identify expressed regions of the Tribolium castaneum genome in unfertilized and fertilized eggs using a whole-genome tiled microarray.
Project description:Using a tiled whole-genome microarray, we found that 58.2% of Tribolium castaneum genes are maternally loaded into eggs. Comparison of known Drosophila melanogaster maternal genes to our results showed widespread conservation of maternal function with T. castaneum. We also found many T. castaneum genes with previously identified gender or tissue specific expression were also maternally loaded into eggs. The microarray design also allowed the detection of 2315 and 4060 novel transcriptionally active regions greater in length than 100 bp in unfertilized and fertilized T. castaneum eggs, respectively. The primary objective of this study was to identify expressed regions of the Tribolium castaneum genome in unfertilized and fertilized eggs using a whole-genome tiled microarray. The whole RNA of 3 samples of virgin laid eggs and 3 samples of fertilized eggs were compaired.
Project description:We identified 429 potential RNA targets of DAZL in the human fetal ovary (padj<0.01), with function in synaptonemal complex formation and recombination (SYCP1, SYCP3, HORMAD1, TRIP13, TEX11), structural maintenance of chromosomes/cohesin formation and spindle assembly checkpoint (SMC1B, RAD21L, MAD2L1), and DNA repair (RAD18, RAD51, RAD54B).
