Plants have a remarkable potential for sustained (indeterminate) postembryonic growth. Following their specification in the early embryo, tissue-specific precursor cells first establish tissues and later maintain them postembryonically. The mechanisms underlying these processes are largely unknown. Here we define local control of oriented, periclinal cell division as the mechanism underlying both the establishment and maintenance of vascular tissue. We identify an auxin-regulated basic helix-loop-helix (bHLH) transcription factor dimer as a critical regulator of vascular development. Due to a loss of periclinal divisions, vascular tissue gradually disappears in bHLH-deficient mutants; conversely, ectopic expression is sufficient for triggering periclinal divisions. We show that this dimer operates independently of tissue identity but is restricted to a small vascular domain by integrating overlapping transcription patterns of the interacting bHLH proteins. Our work reveals a common mechanism for tissue establishment and indeterminate vascular development and provides a conceptual framework for developmental control of local cell divisions.
Chromatin structure and accessibility, and combinatorial binding of transcription factors to regulatory elements in genomic DNA control transcription. Genetic variations in genes encoding histones, epigenetics-related enzymes or modifiers affect chromatin structure/dynamics and result in alterations in gene expression contributing to cancer development or progression. Gliomas are brain tumors frequently associated with epigenetics-related gene deregulation. We perform whole-genome mapping of chromatin accessibility, histone modifications, DNA methylation patterns and transcriptome analysis simultaneously in multiple tumor samples to unravel epigenetic dysfunctions driving gliomagenesis. Based on the results of the integrative analysis of the acquired profiles, we create an atlas of active enhancers and promoters in benign and malignant gliomas. We explore these elements and intersect with Hi-C data to uncover molecular mechanisms instructing gene expression in gliomas.
Obesogenic diets lead to overeating and obesity by inducing the expression of genes involved in hedonic and homeostatic responses in specific brain regions. However, how the effects on gene expression are coordinated in the brain so far remains largely unknown. In our study, we provided mice with access to energy-dense diet, which induced overeating and overweight, and we explored the transcriptome changes across the main regions involved in feeding and energy balance: hypothalamus, frontal cortex, and striatum. Interestingly, we detected two regulatory processes: a switch-like regulation with differentially expressed (DE) genes changing over 1.5-fold and “fine-tuned” subtler changes of genes whose levels correlated with body weight and behavioral changes. We found that genes in both categories were positioned within specific topologically associated domains (TADs), which were often differently regulated across different brain regions. These TADs were enriched in genes relevant for the physiological and behavioral observed changes. Our results suggest that chromatin structure coordinates diet-dependent transcriptional regulation.
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