Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ZFP57 is a regulator of postnatal growth and life-long health

ABSTRACT: Early-life factors, including nutrition, shape long-term health outcomes. Despite the essential role of lactation in maternal nutritional support, the influence of epigenetic factors on lactation and postnatal growth remains poorly understood. Zinc-finger protein 57 (ZFP57), is an epigenetic regulator of genomic imprinting, a process that directs gene expression based on parental origin, playing a vital role in mammalian prenatal growth. Here, we identify a novel function of ZFP57 in the mammary gland, where it serves as a key modulator of postnatal resource control, independently of imprinted genes. ZFP57 regulates multiple aspects of mammary gland functions, including ductal branching and cellular homeostasis. Its absence leads to significant differential gene expression, related to alveologenesis, lactogenesis and milk synthesis, associated with delayed lactation and altered milk composition. This results in life-long impacts on offspring including the development of metabolic syndrome. Cross-fostering reveals intricate dynamics between mother and offspring during lactation. Pups raised by a dam of a different genotype than their birth-mother exhibit exacerbated metabolic features in adulthood. This study shows a novel mechanism responsible for the programming of offspring long-term health by maternal context.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Albert Koulman

PROVIDER: MSV000099723 | MassIVE | Mon Nov 03 01:20:00 GMT 2025

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ZFP57 is a regulator of postnatal growth and life-long health

Project description:Early-life factors, including nutrition, shape long-term health outcomes. Despite the essential role of lactation in maternal nutritional support, the influence of epigenetic factors on lactation and postnatal growth remains poorly understood. Zinc-finger protein 57 (ZFP57), is an epigenetic regulator of genomic imprinting, a process that directs gene expression based on parental origin, playing a vital role in mammalian prenatal growth. Here, we identify a novel function of ZFP57 in the mammary glandI, where it serves as a key modulator of postnatal resource control, independently of imprinted genes. ZFP57 regulates multiple aspects of mammary gland functions, including ductal branching and cellular homeostasis. Its absence leads to significant differential gene expression, related to alveologenesis, lactogenesis and milk synthesis, associated with delayed lactation and altered milk composition. This results in life-long impacts on offspring including the development of metabolic syndrome. Cross-fostering reveals intricate dynamics between mother and offspring during lactation. Pups raised by a dam of a different genotype than their birth mother exhibit exacerbated metabolic features in adulthood, providing additional novel insight into the programming of offspring long-term health by maternal context. This study deepens our understanding of the interplay between epigenetic factors, lactation, and postnatal resource control.

2024-07-31 | GSE248780 | GEO

Effect of lactational high fat diet and metformin on mid-lactation murine mammary gland gene expression

Project description:Maternal health and diet can have important consequences for offspring nutrition and metabolic health. Signals are communicated from the mother to the infant during lactation through milk via macronutrients, hormones and bioactive molecules. In this study we designed experiments to probe the mother-milk-infant triad in the condition of normal maternal health and upon exposure to high fat diet (HFD) with or without concurrent metformin exposure. We examined maternal characteristics, milk composition and offspring metabolic parameters on postnatal day 16, prior to offspring beginning to wean. We found that lactational HFD increased maternal adipose tissue, mammary gland adipocytes, and altered milk lipid composition causing a higher amount of n-6 long chain fatty acids and lower n-3. Offspring of HFD dams were heavier with more body fat during suckling. Metformin exposure decreased maternal glucose and several amino acids. Offspring of met dams were smaller during suckling. Gene expression in the lactating mammary glands was impacted to a greater extent by metformin but both metformin and HFD altered genes related to muscle contraction, indicating that these genes may be more susceptible to lactational stressors. Our study demonstrates the impact of common maternal exposures during lactation on milk composition, mammary gland function and offspring growth with metformin having little capacity to recuse from the effects of a maternal HFD during lactation.

2021-06-04 | GSE176118 | GEO

Expression of milk miRNA during the lactation cycle of the marsupial tammar wallaby (Macropus eugenii)

Project description:High throughput sequencing of miRNAs collected from tammar milk at different time points of lactation showed high levels of miRNA secreted in milk and allowed the identification of differentially expressed milk miRNAs during the lactation cycle as putative markers of mammary gland activity and functional candidate signals to assist growth and timed development of the young. Comparative analysis of miRNA distribution in milk and blood serum suggests that milk miRNAs are primarily expressed from mammary gland rather than transferred from maternal circulating blood, likely through a new putative exosomal secretory pathway.

2015-09-11 | GSE58941 | GEO

Expression of milk miRNA during the lactation cycle of the marsupial tammar wallaby (Macropus eugenii)

2015-09-11 | E-GEOD-58941 | biostudies-arrayexpress

Maternal Nurtritional Programming in the Ovine Mammary Gland

Project description:Developmental programming is the concept that environmental factors, particularly during foetal life, can alter development, metabolism and physiology of an organism and this can have consequences later in life. There is growing interest in developmental programming in livestock species, particularly effects of maternal pregnancy nutrition, which is easy to manipulate. Recent research, using a sheep model, has shown that milk production in ewe offspring may be susceptible to maternal nutritional programming, such that over nutrition (ad libitum) of the pregnant dam, compared with maintenance nutrition, may impair their first lactation performance and result in the weaning of lighter lambs. RNA-seq was performed to identify gene expression differences as a result of maternal nutrition in ewe offspring during their first parity. Samples were collected in late pregnancy and during lactation, allowing us to examine gene expression changes during maturation of the ovine mammary gland. Three biological replicates were sequenced for each of the treatment conditions (maternal nutrition: sub-maintenance, maintenance, and ad libitum) and time points (late pregnancy and lactation). Each biological replicate consisted of RNA from multiple individuals (late pregnancy n=3, lactation n=2).

2015-07-29 | E-GEOD-71424 | biostudies-arrayexpress

RNA-sequencing of milk cells extracted from pre-partum secretions and longitudinally from mature human milk across the first year of lactation

Project description:Changes in mammary cell behavior mediating normal breast development during pregnancy and lactation are poorly understood due to limited availability of breast biopsies during this time. Human milk contains a hierarchy of cells including stem cells, mature milk producing cells (lactocytes) and myoepithelial cells. Here we non-invasively sampled the total epithelial cell population of the lactating mammary gland from mature HM collected from healthy mother/infant dyads during the first year postpartum, and explored temporal changes in the mammary cell transcriptome using RNA sequencing. Comparisons were done with mammary secretions from late pregnancy from the same women and with purchased resting mammary tissue. Distinct gene signatures were found for the different mammary developmental stages examined. Cell adhesion pathways were differentially regulated between the resting gland and pregnancy, whereas immune cell signaling and morphogenesis/cancer pathways differed between lactation and pregnancy or the resting gland, respectively. The transcriptome of lactation remained consistent in the first year postpartum in these successfully lactating women. The gene signatures characteristic of HM cells confirmed lactation genes previously reported in animal models and the HM fat globule. This study identifies key genes and molecular pathways undergoing controlled regulation as the mammary gland transitions from a quiescent into a functional organ, providing experimental targets for the molecular investigation of mammary gland pathologies.

2018-12-26 | GSE85494 | GEO

In utero heat stress alters the offspring epigenome

Project description:Exposure to intrauterine heat stress during late gestation affects offspring performance into adulthood. However, underlying mechanistic links between thermal insult in fetal life and postnatal outcomes are not completely understood. Utilizing RNA Sequencing, this study characterized the mammary gland transcriptome of heifers that were gestated under maternal conditions of heat stress or cooling, i.e., in utero heat stressed (HT) vs. in utero cooled (CL). Mammary tissues were collected from three HT and three CL heifers during their first lactation.

2018-08-30 | GSE119216 | GEO

Breastfeeding infants transmit influenza virus to the mammary glands during feeding [Dataset Part I]

Project description:Influenza virus transmission between mothers and nursing-infants has not been investigated although mothers and infants often develop severe disease. Ferrets are considered the most appropriate model for influenza studies. We investigated influenza transmission in infant and nursing-mother ferrets. Influenza infected infants transmitted virus to mother mammary glands leading to live virus excretion in milk and influenza virus positive mammary gland epithelial cells. Global gene expression analysis showed down-regulation of milk production and induction of breast involution and oncogenesis pathways. Our results provide insight into influenza transmission between mothers and infants which may impact fields of infectious disease, maternal/infant health and neoplasm etiology. Total RNA was obtained from nursing mother ferret mammary glands at days 3/4 and 6/7 post-intranasal kit infection with 10^5 EID50 A/California/07/2009 (H1N1). Total RNA was also collected from uninfected control nursing mother mammary gland tissues (n = 3). Changes in gene expression relative to uninfected tissue controls were then investigated.

2015-09-10 | E-GEOD-63082 | biostudies-arrayexpress

Maternal intra-epithelial lymphocytes support lactogenesis and offspring fitness

Project description:Breastfeeding is an obligatory requirement of mammalian survival. This fundamental process is associated with the remodeling of maternal physiology including the transformation of mammary gland into milk-secreting organ. While adaptive immunity has been associated with the broad control of host physiology, how maternal immunity contributes to organismal remodeling during pregnancy including mammary gland remodeling and function remains largely unknown. Here, we show that maternal adaptive immunity plays a critical role in shaping lactogenesis. Specifically, physiological adaptation to pregnancy is associated with thymic involution and paradoxical enrichment in intraepithelial lymphocyte precursors that no longer migrate to the gut but preferentially accumulate within the mammary gland. Within this compartment the precursors develop as T-bet expressing lymphocytes accumulating within the mammary epithelium in an IL-15 dependent manner. Mammary intra-epithelial lymphocytes control milk production by favoring differentiation of both contractile and milk-secreting cells, thereby affecting offspring fitness. Altogether, this work uncovers a previously unappreciated contribution of the maternal adaptive immune system in organismal remodeling during pregnancy associated with mammary gland development and function.

2025-02-14 | GSE253989 | GEO

Mammary intra-epithelial lymphocytes promote lactogenesis and offspring fitness

Project description:Breastfeeding is an obligatory requirement of mammalian survival. This fundamental process is associated with the adaptation of maternal physiology including the transformation of the mammary gland into a milk-secreting organ. How maternal immunity contributes to mammary gland remodeling and function remains largely unknown. Here, we show that maternal adaptive immunity plays a critical role in shaping lactogenesis. Specifically, physiological adaptation during pregnancy is associated with thymic involution and a paradoxical enrichment in intraepithelial lymphocyte (IEL) precursors that no longer migrate to the gut, but instead preferentially accumulate within the mammary gland. Within this compartment, IEL precursors differentiate into T-bet-expressing unconventional CD8 lymphocytes with a cytotoxic signature which accumulate within the mammary epithelium in an IL-15-dependent manner. Mammary intra-epithelial lymphocytes control milk production by favoring differentiation and maturation of both contractile and milk-secreting cells, thereby promoting offspring fitness. Altogether, this work uncovers a previously unappreciated contribution of the maternal adaptive immune system in organismal remodeling during pregnancy that is associated with mammary gland development and function.

2025-06-04 | GSE280020 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data