Cellular plasticity at the nexus of development and disease

Abstract

In October 2020, the Keystone Symposia Global Health Series hosted a Keystone eSymposia entitled ‘Tissue Plasticity: Preservation and Alteration of Cellular Identity’. The event synthesized groundbreaking research from unusually diverse fields of study, presented in various formats, including live and virtual talks, panel discussions and interactive e-poster sessions. The meeting focused on cell identity changes and plasticity in multiple tissues, species and developmental contexts, both in homeostasis and during injury. Here, we review the key themes of the meeting: (1) cell-extrinsic drivers of plasticity; (2) epigenomic regulation of cell plasticity; and (3) conserved mechanisms governing plasticity. A salient take-home conclusion was that there may be conserved mechanisms used by cells to execute plasticity, with autodegradative activity (autophagy and lysosomes) playing a crucial initial step in diverse organs and organisms.

On the origin of gastric tumours: analysis of a case with intramucosal gastric carcinoma and oxyntic gland adenoma

“…Metaplasia in the stomach is considered to be a response to inflammatory stimuli as well as precancerous lesions [11,12]. Acute inflammatory stimuli caused by DMP-777 or high-dose tamoxifen administration can induce SPEM in mouse models, and the glands immediately recover to normal after removal of stimuli [3,13].…”

A MTA2-SATB2 chromatin complex restrains colonic plasticity toward small intestine by retaining HNF4A at colonic chromatin

“…To perform specialized functions, distinct cell types must maintain unique identities, including cell type-specific transcriptomes. They also need to adapt to changing environments by deploying plasticity in transcription or even cell identity [31][32][33] . The molecular control of cell identity and plasticity is a fundamental question, with scant mechanistic insights.…”