TY  - JOUR
TI  - The folic acid metabolism gene <I>mel-32/Shmt</I> is required for normal cell cycle lengths in <I>Caenorhabditis elegans</I>
AU  - Konrad, KalinD.
AU  - Campbell, RaquelA.
AU  - Thiel, Vanessa
AU  - Sullivan-Brown, Jessica
T2  - The International Journal of Developmental Biology
AB  - 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 mel-32/Shmt is required for normal cell cycle lengths in C. elegans.
PY  - 2018
DO  - 10.1387/ijdb.180023js
VL  - 62
IS  - 9-10
SP  - 641
EP  - 645
J2  - Int. J. Dev. Biol.
LA  - en
SN  - 0214-6282
SN  - 1696-3547
UR  - https://ijdb.ehu.eus/article/180023js
Y2  - 2024/11/23/12:25:37
ER  -