Project description:Investigation of whole genome gene expression level in Pseudozyma antarctica T-34, compared to Ustilago maydis UM521. To clarify the transcriptomic characteristics of Pseudozyma antarctica under the conditions of high MEL production, a DNA microarray of both the strains, Pseudozyma antarctica T-34 and Ustilago maydis UM521 was prepared and analyzed the transcriptomes.
Project description:Investigation of whole genome gene expression level in Pseudozyma antarctica T-34, compared to Ustilago maydis UM521. To clarify the transcriptomic characteristics of Pseudozyma antarctica under the conditions of high MEL production, a DNA microarray of both the strains, Pseudozyma antarctica T-34 and Ustilago maydis UM521 was prepared and analyzed the transcriptomes. A DNA chip study using mRNA from the cultures of Pseudozyma antarctica T-34 and Ustilago maydis UM521 demonstrated the gene expression level of each strain.
Project description:The study aims at deciphering the response of Phaeocystis antarctica under iron limitation and iron supplementation at a transcriptomic level.
Project description:We report the genome wide distribution of the three states of H3K79 methylation (H3K79me1/me2/me3) and H3K27me3 in mouse lineage negative Sca-1 positive Kit positive cells (LSKs), granulocyte macrophage progenitors (GMPs) and LSK derived MLL-AF9 leukemias in the presence or absence of the Af10 OM-LZ domain. Legend- MIT:MSCV-IRES-tdTomato (Empty vector control) and CRE (MIT vector with the Cre recombinase). We examined the H3K79 me1,me2,me3 and H3K27me3 profiles by ChIP-seq in lineage negative Sca-1 positive, Kit positive (LSK) cells, granulocyte macrophage progenitors (GMPs) and bone marrow cells from sacrificed terminally ill secondary MLL-AF9 positive leukemic mice. In case of the MLL-AF9 leukemias, the ChIP-seq experiments were performed in 2 conditions in the presence or absence of the Dot1l interacing octapeptide-motif leucine zipper (OM-LZ) domain of Af10. For the leukemia experiments, leukemias derived from the Af10 OM-LZ homozygous floxed background were transduced with MSCV-IRES-tdTomato control vector (MIT) or its Cre-recombinase expressing counterparts (CRE). Subsequently, we sorted tdTomato positive cells and injected them into sub-lethally irradiated syngenic secondary recipient mice. Seconday leukemias obtained from these MIT or CRE expressing cells were used for ChIP -seq studies.
Project description:Leptotene and zygote (LZ) spematocytes at P11, P16, and P21 were compared by small-RNA-seq. The P21 data has been published under GSE70891. This revealed that, the late piRNA clusters were rarely expressed in P11 LZ spermatocytes, but started to be expressed at P16. Whereas previous reports analysing testicular RNAs showed that "prepachytene" piRNAs are short (25–28 nt) , this study revealed that piRNAs derived from the late piRNA clusters in P16 and P21 LZ spermatocytes contained both short (25–28 nt) and long (29–31 nt) piRNAs.
Project description:Germinal centers (GCs), sites of antibody affinity maturation, are organized into dark (DZ) and light (LZ) zones. Here, we uncovered a B cell intrinsic role for STAT3 in GC DZ and LZ organization. Altered zonal organization of STAT3-deficient GCs dampened GC output of long- lived plasma cells (LL-PCs) but increased memory B cells (MBCs). Tfh-GC B cell interaction drive STAT3 tyrosine 705 and serine 727 phosphorylation in LZ B cells, facilitating their recycling into the DZ. An inducible system confirmed STAT3 is not involved in initiating or maintaining the GC but sustains GC zonal organization by regulating GC B cell recycling. RNAseq and ChIPseq analysis identified genes regulated by STAT3 that are critical for LZ cell recycling and transiting through the DZ proliferation and differentiation phases of the DZ. Thus, STAT3 signaling in B cells controls GC zone organization and recycling, and GC egress of LL- PCs, but negatively regulates MBC output.
Project description:The mechanism through which lymphoma-associated EZH2 gain-of-function mutations disrupt the immune system to initiate malignant transformation is poorly understood. Conditional expression of mutant Ezh2 in germinal center (GC) B-cells provides a competitive advantage to activated B-cells in expanding the GC light zone (LZ) that is not caused by failure to differentiate and exit the GC. Instead, the LZ enlargement is explained by reduced apoptosis of Ezh2 mutant centrocytes, aberrant LZ proliferation, and failure of these centrocytes to re-enter the dark zone (DZ). Ezh2 mutant GCs fail to engage T-cells and to undergo clonal diversification, exhibiting a reduced IgV mutation frequency. Hence the dominant competitive advantage effect of Ezh2 mutation during early stages of transformation is to uncouple GC B-cells from T-cell help checkpoint, which allows GC B-cells entering the LZ to persist and expand regardless of their immunoglobulin status, reflecting the biology of low-grade follicular lymphomas.
Project description:Gene expression analysis performed on FACS sort purified GC LZ and DZ cells of either high and low affinity to identify unique gene signatures. In order to reveal differences between LZ and DZ independent of affinity, we compared a DZ data set (consisting of high and low affinity samples), to a LZ data set (consisting of high and low affinity samples). Analysis revealed distrinct transcription patterns.
