Project description:Genomic imprinting is an epigenetic phenomenon by which certain genes display differential expression in a parent-of-origin-dependent manner. Hundreds of imprinted genes have been identified from several plant species. Here we identified, with a high level of confidence, 208 imprinted candidates from rice. Imprinted genes of rice showed limited association to the transposable elements, which contrasts with findings from Arabidopsis. Generally, imprinting in rice is conserved within species, but intraspecific variation was detected as well.
Project description:In Arabidopsis thaliana, DNA-dependent RNA polymerase IV (Pol IV) is required for the formation of transposable element (TE)-derived small RNA (sRNA) transcripts. These transcripts are processed by DICER-LIKE3 into 24-nt small interfering RNAs (siRNAs) that guide RNA-directed DNA methylation. In the pollen grain, Pol IV is also required for the accumulation of 21/22-nt epigenetically activated siRNAs (easiRNAs), which likely silence TEs via post-transcriptional mechanisms. Despite this proposed role of Pol IV, its loss of function in Arabidopsis does not cause a discernable pollen defect. Here, we show that the knockout of NRPD1, encoding the largest subunit of Pol IV in the Brassicaceae species Capsella rubella, caused post-meiotic arrest of pollen development at the microspore stage. As in Arabidopsis, all TE-derived siRNAs were 2 depleted in Capsella nrpd1 microspores. In the wild-type background, the same TEs produced 21/22-nt and 24-nt siRNAs; these processes required Pol IV activity. Arrest of Capsella nrpd1 microspores was accompanied by the deregulation of genes targeted by Pol IV-dependent siRNAs. TEs were much closer to genes in Capsella rubella compared to Arabidopsis thaliana, perhaps explaining the essential role of Pol IV in pollen development in Capsella. Our discovery that Pol IV is functionally required in Capsella microspores emphasizes the relevance of investigating different plant models.
Project description:The seeds of angiosperms are comprised of three main tissues--the seed coat, embryo, and endosperm--whose coordinated development will enable the next generation to disperse with sufficient maternal resources and germinate when conditions are favorable. We use high-throughput RNA sequencing technology to characterize the developmental dynamics of gene expression in whole seeds resulting from a compatible cross between two species of the Mimulus guttatus complex.We find that development in ovules and seeds involves the activation of the majority of annotated genes in M. guttatus (64-67%), and the differential expression over time of 6,691 genes, including 424 transcription factors. Most of the genes we detected (69%) were expressed at all stages, from ovules to heart-stage embryo seeds. We also detected and validated four genes exhibiting paternally-biased expression (MDB13, ATXR5, DnaJ and BGAL11). Intriguingly, three of our validated PEGs are have imprinted homologues in other plant species, suggesting that these proteins perform a shared role in endosperm development among distantly related plant taxa. Additionally, the overlap in gene expression profiles between stages of development suggests that most genes fulfill multiple developmental and biological roles. Future analyses should examine whether different regions of the seed (embryo, endosperm, and seed coat) have unique patterns of gene expression, and the extent to which spatial coordination and regulation of gene expression may play a role in regulating seed development.
Project description:Inborn defects in DNA repairare associated with complex developmental disorders whose causal mechanisms are poorly understood. Using an in vivo biotinylation tagging approach in mice, we show that the nucleotide excision repair (NER) structure-specific endonuclease ERCC1-XPF complex interacts with the insulator binding protein CTCF, the cohesin subunits SMC1A and SMC3 and with MBD2; the factors co-localize with ATRX at the promoters and control regions (ICRs) of imprinted genes during postnatal hepatic development. Loss of Ercc1or exposure to mitomycin C triggers the localization of CTCF to heterochromatin, the dissociation of the CTCF-cohesin complex and ATRXfrom promoters and ICRs,altered histone marks and the aberrant developmental expression of imprinted genes without altering DNA methylation. We propose that ERCC1-XPF cooperates with CTCF and the cohesinto facilitatet he developmental silencing of imprinted genes and that persistent DNA damage triggers chromatin changes that affect gene expression programs associated with NER disorders.