Antisense Knockouts of Genes in the Folate Pathway and Effects on Neural Tube Development

<ol> <li>To determine if knocking out 5,10-methyltetrahydrofolate reductase (MTHFR) activity in mouse embryos in vitro produces neural tube defects;
<li>To determine if addition of exogenous 5-methyltetrahydrofolate is able to overcome the lack of MTHFR activity and produce closed neural tubes in mouse embryos treated in vitro;
<li>To determine if addition of exogenous methionine is able to overcome the lack of MTHFR activity and produce closed neural tubes in mouse embryos treated in vitro;
<li>To determine if knocking out methionine synthase (MS) activity in mouse embryos in vitro produces neural tube defects;
<li>To determine if addition of exogenous methionine is able to overcome the lack of MS activity and produce closed neural tubes in mouse embryos treated in vitro;
<li>To determine if exogenous vitamin B12 is able to overcome the lack of MS activity and produced closed neural tubes in mouse embryos treated in vitro;
<li>To determine if knocking out methionine adenosyltransferase (MAT) activity in mouse embryos in vitro produces neural tube defects;
<li>To determine if addition of exogenous methionine is able to overcome the lack of MAT activity and produce closed neural tubes in mouse embryos treated in vitro;
<li>To determine if addition of exogenous 5-methyltetrahydrofolate is able to overcome the lack of MAT activity and produce closed neural tubes in mouse embryos treated in vitro</ol>