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Khatoon, U.

Publications and source records attributed to Khatoon, U..

2 recordsLinked to original sources

Unravelling cotton RNAseq repositories to the fiber development specific modules and their alliance with the fiber-related traits

Cotton fiber development is still an intriguing question to understand the fiber commitment and development. Here, we remapped >350 publicly available cotton RNA sequencing data on recently published cotton genome with [~]400 fold coverage. The differentially expressed genes were clustered in six modules whose functions are specific to commitment, initiation, elongation and Secondary Cell Wall (SCW) fiber development stages. Gene Ontology analysis of commitment and initiation specific modules suggests enrichment of genes involved in organ development. The modules specific for elongation and SCW showed significant enrichment of hydroxyproline-rich proteins and hydrolases. Transcription factors (TFs) binding frequency of defined modules suggested that homeodomain, MYB and NAC expresses at commitment stages but their expression was governed by other TFs. We also mined the stage-specific transcriptional biomarker and Exclusively Expressed Transcripts (EETs) for fiber. These EETs were positively selected during fiber evolution and cotton domestication. The extensive expression profiling of six EETs in 100 cotton genotypes at different fiber developmental stages using nCounter assay and their correlation with eight fiber-related suggests that several EETs are correlated with different fiber quality-related traits. Thus, our study reveals several important genes and pathways that may be important for cotton fiber development and future improvement of cotton.

plant biology↗

BET inhibition prevents aberrant RUNX1 and ERG transcription in STAG2 mutant leukaemia cells.

Mutations in the subunits of the cohesin complex, particularly in the STAG2 subunit, have been identified in a range of myeloid malignancies, but it is unclear how these mutations progress leukaemia. Here, we created isogenic K562 erythromyeloid leukaemia cells with and without the known leukemic STAG2 null mutation, R614*. STAG2 null cells acquired stem cell and extracellular matrix gene expression signatures that accompanied an adherent phenotype. Chromatin accessibility was dramatically altered in STAG2 null K562 cells, consistent with gene expression changes. Enhanced chromatin accessibility was observed at genes encoding hematopoietic transcription factors, ERG and RUNX1. Upon phorbol 12-myristate 13-acetate (PMA)-induced megakaryocytic differentiation, STAG2-null cells showed precocious spike in RUNX1 transcription from its P2 promoter. A similar precocious spike was observed in transcription of ERG. Interestingly, spikes in RUNX1-P2 and ERG only occurred as immediate early response to differentiation induction. Treatment of STAG2 null cells with enhancer-blocking BET inhibitor, JQ1, dampened precocious RUNX1 P2 expression and led to a complete loss of RUNX1 P1 and ERG transcription during PMA stimulation in both parental and STAG2 null K562 cells. These results suggest that precocious RUNX1 and ERG expression in STAG2 null cells is enhancer-driven. Furthermore, JQ1 treatment reduced stem cell-associated KIT expression in STAG2 null cells. We conclude that STAG2 depletion in leukemic cells amplifies an enhancer-driven transcriptional response to differentiation signals, and this characteristic is dampened by BET inhibition. The results have relevance to the development of therapeutic strategies for myeloid leukaemia

cancer biology↗