Shreeta Chakraborty

Keywords nuclear organization gene regulation epigenetics CTCF FGF Get full text access Log in, subscribe or purchase for full access. References 1. Long, H.K. ∙ Prescott, S.L. ∙ Wysocka, J. Ever-changing landscapes: transcriptional enhancers in development and evolution Cell. 2016; 167:1170-1187 2. Furlong, E.E.M. ∙ Levine, M. Developmental enhancers and chromosome topology Science. 2018; 361:1341-1345 3. Schoenfelder, S. ∙ Fraser, P. Long-range enhancer-promoter contacts in gene expression control Nat.

Abstract Chromatin domain boundaries delimited by CTCF motifs can restrict the range of enhancer action. However, disruption of domain structure often results in mild gene dysregulation and thus predicting the impact of boundary rearrangements on animal development remains challenging. Here, we tested whether structural perturbation of a chromatin domain with multiple developmental regulators can result in more acute gene dysregulation and severe developmental phenotypes.

Endothelial nitric-oxide synthase (eNOS) and its bioactive product, nitric oxide (NO), mediate many endothelial cell functions, including angiogenesis and vascular permeability. For example, vascular endothelial growth factor (VEGF)-mediated angiogenesis is inhibited upon reduction of NO bioactivity both in vitro and in vivo. Moreover, genetic disruption or pharmacological inhibition of eNOS attenuates angiogenesis during tissue repair, resulting in delayed wound closure.