Maternal Vitamin and Mineral Supplementation and Rate of Maternal Weight Gain Affects Placental Expression of Energy Metabolism and Transport-Related Genes

Author:

Diniz Wellison J. S.ORCID,Reynolds Lawrence P.ORCID,Borowicz Pawel P.,Ward Alison K.ORCID,Sedivec Kevin K.,McCarthy Kacie L.ORCID,Kassetas Cierrah J.,Baumgaertner Friederike,Kirsch James D.,Dorsam Sheri T.,Neville Tammi L.ORCID,Forcherio J. Chris,Scott Ronald R.,Caton Joel S.,Dahlen Carl R.ORCID

Abstract

Maternal nutrients are essential for proper fetal and placental development and function. However, the effects of vitamin and mineral supplementation under two rates of maternal weight gain on placental genome-wide gene expression have not been investigated so far. Furthermore, biological processes and pathways in the placenta that act in response to early maternal nutrition are yet to be elucidated. Herein, we examined the impact of maternal vitamin and mineral supplementation (from pre-breeding to day 83 post-breeding) and two rates of gain during the first 83 days of pregnancy on the gene expression of placental caruncles (CAR; maternal placenta) and cotyledons (COT; fetal placenta) of crossbred Angus beef heifers. We identified 267 unique differentially expressed genes (DEG). Among the DEGs from CAR, we identified ACAT2, SREBF2, and HMGCCS1 that underlie the cholesterol biosynthesis pathway. Furthermore, the transcription factors PAX2 and PAX8 were over-represented in biological processes related to kidney organogenesis. The DEGs from COT included SLC2A1, SLC2A3, SLC27A4, and INSIG1. Our over-representation analysis retrieved biological processes related to nutrient transport and ion homeostasis, whereas the pathways included insulin secretion, PPAR signaling, and biosynthesis of amino acids. Vitamin and mineral supplementation and rate of gain were associated with changes in gene expression, biological processes, and KEGG pathways in beef cattle placental tissues.

Funder

North Dakota State Board of Agricultural Research and Education

Publisher

MDPI AG

Subject

Genetics(clinical),Genetics

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