A high glucose level associated with maternal diabetes has been identified as a risk factor for fetal neural tube defects (NTD). The failure to successfully complete the complex neurulation process is possibly related to the loss of protection for cellular homeostasis resulting in organelle stress. Mitochondrial dysfunction and endoplasmic reticulum stress in the developing endothelium have been identified as significant components in diabetic embryopathy. Myristoylated Alanine-Rich C Kinase Substrate (MARCKS) is a critical protein involved in fetal neural development. This study investigated the regulation and biological activity of MARCKS and its role in protecting neuroepithelial cell organelles during neurulation. Furthermore, the effects of the acetylation/phosphorylation/deacetylation of MARCKs by Tip60 and sirtuin 2 were examined with respect to the protein’s protective functionality. The dataset includes immunoblot/immunofluorescent/electronmicroscopy images and graphs.
Data and figures are provided on the effects of fluoxetine, a selective serotin reuptake inhibitor (SSRI) antidepressant, on the gut microbiome and metabolome in a rat model to better understand the effect of this drug on women during gestation and lactation. Throughout pregnancy and lactation, female rats received the SSRI fluoxetine or vehicle. High resolution 16S ribosomal RNA marker gene sequencing and targeted metabolic analysis were used to assess the fecal microbiome and metabolic availability, respectively.