Project description:In cucurbits, CmWIP1 is a master gene controlling sex determination. To bring new insight in the function of CmWIP1, we investigated two Arabidopsis WIP proteins, AtWIP1 and AtWIP2. Using an inducible system we showed that WIPs. are powerful inhibitor of growth and inducer of cell death. Bioproject :
Project description:Analyis gene expression in crc-1 knu-1 compared with knu-1 Initiation of the carpel primordia is marked by the termination of floral stem cells. Although genetic evidences have suggested that the YABBY gene CRABS CLAW (CRC) regulates the development of carpel, as well as the floral meristem determinacy as a target of the homeotic protein AGAMOUS, the underlying mechanism remains unclear. Here we show that the tetraspanin-encoding gene TONADO2 (TRN2) and the auxin biosynthesis gene YUCCA4 (YUC4) act as downstream targets of CRC.
Project description:Purpose: Determine whether sex-determining genes are bivalent at the bipotential stage, poised between the testis and ovary fate, and whether H3K4me3 and H3K27me3 resolve into sex-specific patterns after sex determination, contributing to the canalization and stabilization of either the testis or ovary fate. Methods: XX and XY supporting cells of the gonad were FACS-purified before sex determination (at E10.5) and after sex determination (at E13.5), and submitted to ChIP-seq for H3K4me3, H3K27me3 and H3 as a means to normalize across cell populations. Results: We found that key sex-determining genes are bivalent at the bipotential stage. Genes that are upregulated affter sex determination are stripped of their repressive H3K27me3 mark, whereas repressed genes that promote the alternate pathway remain bivalent even after sex determination.
Project description:The influence of environmental factors, especially temperature, on sex ratio is of great significance to elucidate the mechanism of sex determination. However, the molecular mechanisms by which temperature affects sex determination remains unclear, although a few candidate genes have been found to play a role in the process. In this study, we conducted transcriptome analysis of the effects induced by high temperature on zebrafish during gonad differentiation period. 1171, 1022 and 2921 differentially expressed genes (DEGs) between high temperature and normal temperature were identified at 35, 45 and 60 days post-fertilization (dpf) respectively, revealing that DNA methyltransferases (DNMTs) and heat shock proteins (HSPs) were involved in the heat-exposed sex reversal. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway that were enriched in individuals after heat treatment included Fanconi anemia pathway, cell cycle, oocyte meiosis and homologous recombination. These results provide insights into the network of genes involved in heat-induced masculinization, and improve our understanding the molecular mechanisms of vertebrate sex determination.
Project description:Gene expression in early animal embryogenesis is in large part controlled post-transcriptionally. Maternally-contributed microRNAs may therefore play important roles in early development. We have elucidated a major biological role of the nematode mir-35 family of maternally-contributed, essential microRNAs. We show that this microRNA family regulates the sex determination pathway at multiple levels, acting both upstream and downstream of her-1 to prevent aberrantly activated male developmental programs in hermaphrodite embryos. The predicted target genes that act downstream of the mir-35 family in this process, sup-26 and nhl-2, both encode RNA binding proteins, thus delineating a previously unknown post-transcriptional regulatory subnetwork within the well-studied sex determination pathway of C. elegans. Repression of nhl-2 by the mir-35 family is not only required for proper sex determination but also for viability, showing that a single microRNA target site can be essential. Since sex determination in C. elegans requires zygotic gene expression to read the sex chromosome karyotype, early embryos must remain gender-naïve; our findings show that the mir-35 family microRNAs act in the early embryo to function as a developmental timer that preserves naïveté and prevents premature deleterious developmental decisions. The mir-35 family of microRNAs is essential for development. The mir-35-41(nDf50) allele deleted 7 of 8 mir-35 family members, and presents a hypomorphic phenotype in which embryonic lethality is temperature sensitive. To characterize the molecular phenotype associated with loss of mir-35 family function, we profiled gene expression in mir-35-41(nDf50) mutant embryos at both permissive (20) and restrictive (25) temperatures. (Refer to A microRNA family exerts maternal control on sex determination in C. elegans)
Project description:Gene expression in early animal embryogenesis is in large part controlled post-transcriptionally. Maternally-contributed microRNAs may therefore play important roles in early development. We have elucidated a major biological role of the nematode mir-35 family of maternally-contributed, essential microRNAs. We show that this microRNA family regulates the sex determination pathway at multiple levels, acting both upstream and downstream of her-1 to prevent aberrantly activated male developmental programs in hermaphrodite embryos. The predicted target genes that act downstream of the mir-35 family in this process, sup-26 and nhl-2, both encode RNA binding proteins, thus delineating a previously unknown post-transcriptional regulatory subnetwork within the well-studied sex determination pathway of C. elegans. Repression of nhl-2 by the mir-35 family is not only required for proper sex determination but also for viability, showing that a single microRNA target site can be essential. Since sex determination in C. elegans requires zygotic gene expression to read the sex chromosome karyotype, early embryos must remain gender-naïve; our findings show that the mir-35 family microRNAs act in the early embryo to function as a developmental timer that preserves naïveté and prevents premature deleterious developmental decisions. The mir-35 family of microRNAs is essential for development. The mir-35-41(nDf50) allele deleted 7 of 8 mir-35 family members, and presents a hypomorphic phenotype in which embryonic lethality is temperature sensitive. To characterize the molecular phenotype associated with loss of mir-35 family function, we profiled gene expression in mir-35-41(nDf50) mutant embryos at both permissive (20) and restrictive (25) temperatures. (Refer to A microRNA family exerts maternal control on sex determination in C. elegans)
Project description:Purpose: In this study we employed unbiased, genome-wide techniques to identify regulatory elements during murine sex determination. Methods: We performed ATAC-seq on 60K FACS-purified XX and XY gonadal cells before and after sex determination to map nucleosome depleted regions (NDRs) indicative of regulatory elements. To determine whether these are active enhancers, we performed ChIP-seq for H3K27ac, a histone modification that marks active enhancers in both sexes and time points. Transient transgenics was performed on select enhancers to determine whether they are functional in gonads during the sex determination stage. Results: We have produced a genome wide map of potential regulatory elements and active enhancers during the process of murine sex determination. Furthermore, we validated the power of our dataset by identifying a novel enhancer downstream of Bmp2, a female-specific gene. Conclusions: This work supplies a powerful resource for identifying chromatin regulatory elements active during mammalian sex determination.