| Literature DB >> 30753836 |
Heath E Johnson1, Jared E Toettcher2.
Abstract
The Erk mitogen-activated protein kinase plays diverse roles in animal development. Its widespread reuse raises a conundrum: when a single kinase like Erk is activated, how does a developing cell know which fate to adopt? We combine optogenetic control with genetic perturbations to dissect Erk-dependent fates in the early Drosophila embryo. We find that Erk activity is sufficient to "posteriorize" 88% of the embryo, inducing gut endoderm-like gene expression and morphogenetic movements in all cells within this region. Gut endoderm fate adoption requires at least 1 h of signaling, whereas a 30-min Erk pulse specifies a distinct ectodermal cell type, intermediate neuroblasts. We find that the endoderm-ectoderm cell fate switch is controlled by the cumulative load of Erk activity, not the duration of a single pulse. The fly embryo thus harbors a classic example of dynamic control, where the temporal profile of Erk signaling selects between distinct physiological outcomes.Entities:
Keywords: Drosophila; Erk; cell signaling; development; differentiation; dynamics; optogenetics
Mesh:
Year: 2019 PMID: 30753836 PMCID: PMC6394837 DOI: 10.1016/j.devcel.2019.01.009
Source DB: PubMed Journal: Dev Cell ISSN: 1534-5807 Impact factor: 12.270