Literature DB >> 32446291

How do signaling and transcription factors regulate both axis elongation and Hox gene expression along the anteroposterior axis?

Seiji Saito1, Takayuki Suzuki2.   

Abstract

In vertebrates, vertebral primordia, called somites, are formed from the head to the tail along the anteroposterior axis of the body during development. The presomitic mesoderm (PSM), which differentiates into somites, is formed by continuous supply of new cells derived from the caudal lateral epiblast (CLE), resulting in body axis posterior elongation. Previous studies of mutants identified genes for posterior extension and vertebral patterning along the anteroposterior axis. Hox gene has been extensively investigated for its expression pattern and transcriptional regulation. In recent years, to elucidate the mechanism that controls the expression patterns of Hox genes, researchers have not only searched for enhancer regions and the transcription factors that bind to them but have also investigated chromatin structure, epigenetics and non-coding RNA associated with Hox gene expression. These new findings reveal that the previously identified genes essential for posterior body axis elongation of the embryo determine positional information along the anteroposterior axis by induction of Hox genes via enhancer regions. In this review, we focus on genes that control posterior elongation and vertebral patterning along the anteroposterior axis in the PSM and CLE. We first describe the mechanism of maintenance of the stem cell-like cell populations at the CLE, which is essential for the posterior elongation of the embryo. Next, the factors involved in posterior region formation and patterning of the vertebra are described. Finally, we discuss the regulatory mechanism of Hox gene expression and the mechanism that is responsible for the differences in skeletal pattern between species.
© 2020 Japanese Society of Developmental Biologists.

Keywords:  NMPs; anteroposterior axis; enhancer; hox; vertebral formula

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Year:  2020        PMID: 32446291     DOI: 10.1111/dgd.12682

Source DB:  PubMed          Journal:  Dev Growth Differ        ISSN: 0012-1592            Impact factor:   2.053


  1 in total

1.  Akt1 Decreases Gcn5 Protein Stability through Regulating The Ubiquitin-Proteasome Pathway in Mouse Embryonic Fibroblasts.

Authors:  Da Som Jeong; Yu Cheon Kim; Ji Hoon Oh; Myoung Hee Kim
Journal:  Cell J       Date:  2022-01       Impact factor: 3.128

  1 in total

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