A quantitative model of developmental RTK signaling.

TitleA quantitative model of developmental RTK signaling.
Publication TypeJournal Article
Year of Publication2018
AuthorsGoyal, Y, Schüpbach, T, Shvartsman, SY
JournalDev Biol
Volume442
Issue1
Pagination80-86
Date Published2018 10 01
ISSN1095-564X
KeywordsAnimals, Body Patterning, Drosophila, Drosophila Proteins, Gene Expression Regulation, Developmental, Protein-Tyrosine Kinases, Proto-Oncogene Proteins p21(ras), Receptor Protein-Tyrosine Kinases, Signal Transduction
Abstract

<p>Receptor tyrosine kinases (RTKs) control a wide range of developmental processes, from the first stages of embryogenesis to postnatal growth and neurocognitive development in the adult. A significant share of our knowledge about RTKs comes from genetic screens in model organisms, which provided numerous examples demonstrating how specific cell fates and morphologies are abolished when RTK activation is either abrogated or significantly reduced. Aberrant activation of such pathways has also been recognized in many forms of cancer. More recently, studies of human developmental syndromes established that excessive activation of RTKs and their downstream signaling effectors, most notably the Ras signaling pathway, can also lead to structural and functional defects. Given that both insufficient and excessive pathway activation can lead to abnormalities, mechanistic analysis of developmental RTK signaling must address quantitative questions about its regulation and function. Patterning events controlled by the RTK Torso in the early Drosophila embryo are well-suited for this purpose. This mini review summarizes current state of knowledge about Torso-dependent Ras activation and discusses its potential to serve as a quantitative model for studying the general principles of Ras signaling in development and disease.</p>

DOI10.1016/j.ydbio.2018.07.012
Alternate JournalDev. Biol.
PubMed ID30026122
PubMed Central IDPMC6501586
Grant ListR01 GM077620 / GM / NIGMS NIH HHS / United States
R01 GM086537 / GM / NIGMS NIH HHS / United States