New findings shed light on the connection between vulva and uterus development.
A collaboration with the Hajnal group at the University of Zurich has uncovered a specific function of the epithelial growth factor receptor (EGFR) in the anchor cell (AC) during vulval lumen morphogenesis.
One of the key challenges in the field of developmental biology is understanding how cells change their shape and alter their behaviour to form organs, a process termed ‘morphogenesis’. While several models for morphogenetic processes exist, a powerful yet simple experimental model of Caenorhabditis elegans (C. elegans) vulva development has yet to be realized. To allow a detailed analysis of morphogenesis in C. elegans, worms must be immobilized for long periods of time. In this regard, microfluidic platforms are attractive alternatives to conventional agar pads, since they can house and immobilize worms, whilst allowing normal growth and molting. Although several microfluidic platforms have been developed for such a purpose, most are ill-suited to maintaining a stable worm orientation over extended timescale. To solve this problem, Simon Berger and colleagues developed a novel microfluidic platform (link) that allows the live imaging of multiple worms across multiple larval stages.
In a paper published in Development, the researchers use this novel microfluidic platform to investigate the specific function of the uterine anchor cell (AC) during vulval lumen morphogenesis. As can be seen below, worms can be loaded and trapped in simple manner, with a low-height region (shown in red) being used to locate worms in an imaging zone. Subsequently, the authors investigated the functions of LET-23 and LIN-4, which are EGFR tyrosine kinase and EGF encoded in the C. elegans genome, respectively, with data verifying that LET-23 expression is required for the precise alignment of the AC with the invaginating vulval cells, and indicating that LET-23 signaling in the AC governs the organization of vulval-uterine junctions and the establishment of an actin scaffold. Overall, the study demonstrates for the first time that LET-23 signaling is necessary to connect the vulva to the uterus.
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