Newborn pig uterus gene expression changes in response to lactocrine insufficiency from birth

Maternal effects on offspring phenotype do not end at birth. Bioactive factors are transmitted from mother to nursing offspring through colostrum, which is known as lactocrine programming. The lactocrine hypothesis posits that disruption of lactocrine signaling from birth will have both short- and long-term effects on the postnatal developmental program with lasting consequences. Previous research established that lactocrine insufficiency from birth in pigs, indicated by reduced serum immunoglobulin immunocrit (iCrit) ratios in nursing piglets on the day of birth (postnatal day 0, PND0), altered the postnatal uterine developmental program and reduced lifetime fecundity in adult, neonatally lactocrine insufficient females. To determine the effects of lactocrine insufficiency on uterine development in the rapid growth phase, we performed RNA sequencing in six high-low iCrit pairs in PND14 gilt littermates. High-quality RNA-seq reads were mapped to the porcine reference genome, and the expression levels were quantified in the uterus transcriptome. We identified 148 (1.1% of expressed genes) differentially expressed genes (DEGs) between the high and low iCrit groups at P < 0.05, including the the FOXA2 gene, which was known to be downregulated in low-iCrit uterus samples. Gene ontology analysis reveals that immune-related functions, including the complement pathways are up-regulated in the low iCrit group. Overall design: Crossbred gilts, born and maintained at the US Meat Animal Research Center (Clay Center, NE), were assigned to low (n=6) or high (n=6) iCrit groups based on iCrit ratio values determined on PND0. To characterize lactocrine effects on the PND14 uterine transcriptome in low/high iCrit gilts, 6 pairs of low and high iCrit gilts from the same litters were euthanized and uterus samples were collected on PND14, following by RNA extraction, stranded mRNAseq library construction and sequencing.