Skip to Content
Merck
  • The cell surface hyaluronidase TMEM2 plays an essential role in mouse neural crest cell development and survival.

The cell surface hyaluronidase TMEM2 plays an essential role in mouse neural crest cell development and survival.

PLoS genetics (2022-07-16)
Toshihiro Inubushi, Yuichiro Nakanishi, Makoto Abe, Yoshifumi Takahata, Riko Nishimura, Hiroshi Kurosaka, Fumitoshi Irie, Takashi Yamashiro, Yu Yamaguchi
ABSTRACT

Hyaluronan (HA) is a major extracellular matrix component whose tissue levels are dynamically regulated during embryonic development. Although the synthesis of HA has been shown to exert a substantial influence on embryonic morphogenesis, the functional importance of the catabolic aspect of HA turnover is poorly understood. Here, we demonstrate that the transmembrane hyaluronidase TMEM2 plays an essential role in neural crest development and the morphogenesis of neural crest derivatives, as evidenced by the presence of severe craniofacial abnormalities in Wnt1-Cre-mediated Tmem2 knockout (Tmem2CKO) mice. Neural crest cells (NCCs) are a migratory population of cells that gives rise to diverse cell lineages, including the craniofacial complex, the peripheral nervous system, and part of the heart. Analysis of Tmem2 expression during NCC formation and migration reveals that Tmem2 is expressed at the site of NCC delamination and in emigrating Sox9-positive NCCs. In Tmem2CKO embryos, the number of NCCs emigrating from the neural tube is greatly reduced. Furthermore, linage tracing reveals that the number of NCCs traversing the ventral migration pathway and the number of post-migratory neural crest derivatives are both significantly reduced in a Tmem2CKO background. In vitro studies using Tmem2-depleted mouse O9-1 neural crest cells demonstrate that Tmem2 expression is essential for the ability of these cells to form focal adhesions on and to migrate into HA-containing substrates. Additionally, we show that Tmem2-deficient NCCs exhibit increased apoptotic cell death in NCC-derived tissues, an observation that is corroborated by in vitro experiments using O9-1 cells. Collectively, our data demonstrate that TMEM2-mediated HA degradation plays an essential role in normal neural crest development. This study reveals the hitherto unrecognized functional importance of HA degradation in embryonic development and highlights the pivotal role of Tmem2 in the developmental process.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Monoclonal Anti-Vinculin antibody produced in mouse, clone VIN-11-5, ascites fluid
Sigma-Aldrich
Anti-Vinculin antibody, Mouse monoclonal, clone hVIN-1, purified from hybridoma cell culture
Millipore
ANTI-FLAG® antibody produced in rabbit, affinity isolated antibody, buffered aqueous solution
Sigma-Aldrich
Anti-TMEM2 antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
O9-1 Mouse Cranial Neural Crest Cell Line, stably expresses stem cell markers and neural crest markers
Sigma-Aldrich
Anti-phospho-Histone H3 (Thr3) Antibody, clone JY325, rabbit monoclonal, clone JY325, from rabbit
Sigma-Aldrich
Anti-Actin, α-Smooth Muscle antibody, Mouse monoclonal, clone 1A4, purified from hybridoma cell culture
Roche
In Situ Cell Death Detection Kit, Fluorescein, sufficient for ≤50 tests, suitable for detection
Sigma-Aldrich
Monoclonal ANTI-FLAG® BioM2 antibody produced in mouse, clone M2, purified immunoglobulin, buffered aqueous glycerol solution