Notch Signalling Under Maternal-to-Zygotic Transition

Fly (Austin). 2022 Dec;16(1):347-359. doi: 10.1080/19336934.2022.2139981.

Abstract

The development of all animal embryos is initially directed by the gene products supplied by their mothers. With the progression of embryogenesis, the embryo's genome is activated to command subsequent developments. This transition, which has been studied in many model animals, is referred to as the Maternal-to-Zygotic Transition (MZT). In many organisms, including flies, nematodes, and sea urchins, genes involved in Notch signaling are extensively influenced by the MZT. This signaling pathway is highly conserved across metazoans; moreover, it regulates various developmental processes. Notch signaling defects are commonly associated with various human diseases. The maternal contribution of its factors was first discovered in flies. Subsequently, several genes were identified from mutant embryos with a phenotype similar to Notch mutants only upon the removal of the maternal contributions. Studies on these maternal genes have revealed various novel steps in the cascade of Notch signal transduction. Among these genes, pecanex and almondex have been functionally characterized in recent studies. Therefore, in this review, we will focus on the roles of these two maternal genes in Notch signaling and discuss future research directions on its maternal function.

Keywords: Notch signaling; almondex; early embryogenesis; maternal effect; maternal-to-zygotic transition; pecanex.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Embryonic Development / genetics
  • Gene Expression Regulation, Developmental*
  • Genome
  • Humans
  • Signal Transduction
  • Zygote* / metabolism

Grants and funding

This work was supported by the Japanese Ministry of Education Culture under the Japan Society for the Promotion of Science (JSPS 21H02488 21H05782) KAKENHI Grant Number JP18K14697; Toyota Physical and Chemical Research Institute under 2020 Toyota Riken Scholar Program to T. Y.