Document Type

Article

Publication Date

2018

Abstract

Neural tube defects are common and serious birth defects in which the brain and/or spinal cord are exposed outside the body. Supplementation of foods with folic acid, an essential vitamin, is linked to a lower risk of neural tube defects; however, the mechanisms by which folic acid influence neural tube defect risk are unclear. Our research seeks to identify the basic cellular roles of known folic acid metabolism genes during morphogenesis using the roundworm Caenorhabditis elegans (C. elegans) as a simple model system. Here, we used live imaging to characterize defects in embryonic development when mel-32 is depleted. mel-32 is an essential folic acid metabolism gene in C. elegans and a homolog to the mammalian enzyme serine hydroxymethyltransferase (Shmt). Disruption of mel-32 resulted in a doubling or tripling of cell cycle lengths and a lack of directed cell movement during embryogenesis. However, the order of cell divisions, as determined by lineage analysis, is unchanged compared to wild type embryos. These results suggest that mel32/Shmt is required for normal cell cycle lengths in C. elegans.

Publication Title

International Journal of Developmental Biology

ISSN

0214-6282

Publisher

University of the Basque Country Press

Volume

62

Issue

9-10

First Page

641

Last Page

645

DOI

10.1387/ijdb.180023js

Available for download on Thursday, December 12, 2019

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