Single gene causes embryo notochord deformity in zebrafish, study reveals

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Can a single protein-encoding gene determine whether a vertebrate embryo develops normally? Yes, according to Osaka Metropolitan University researchers, who found that suppression of Pcdh8 is essential for the notochord to elongate properly in zebrafish.

Graduate School of Medicine Dr. Masatake Kai and Professor Makoto Kondo focused on this paraxial protocadherin (PAPC), which is excluded when dividing cells migrate and form the notochord in the embryo. The findings were published in Scientific Reports.

In the experiments with zebrafish embryos, when this PAPC is not excluded, the cells do not move to the appropriate location, preventing the notochord from elongating to its proper length.

The researchers suggest that the role this gene plays in controlling cell proliferation when expressed might lead to novel tumor therapies in humans.

"In this case, the results were obtained using zebrafish, but it is possible that a similar mechanism may also be at work in mammals," Professor Kondo stated. "We hope to make more progress in understanding the complex mechanisms that give rise to the forms of living things."

More information: Masatake Kai et al, Suppression of Pcdh8/paraxial protocadherin is required for efficient neighbor exchange in morphogenetic cell movement during zebrafish notochord formation, Scientific Reports (2024). DOI: 10.1038/s41598-024-76762-7

Journal information: Scientific Reports

Provided by Osaka Metropolitan University