PAe000351_mzXML_200906162257
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Instrument
ORGANISM(S): Crap, Leptospira_interrogans_serovar_copenhageni, Leptospira_interrogans_serovar_lai
DISEASE(S): Not Available
SUBMITTER: 
Z. Sun
PROVIDER: GPM11200004579 | GPMDB |
REPOSITORIES: GPMDB
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Project description:Background: Iron deficiency anemia is a major challenge in in both human health and animal husbandry. Disrupted bile acid metabolism is a key characteristic among people with anemia. However, effects and mechanisms of iron deficiency on bile acid metabolism remain unclear. N6-methyladenine (m6A) is the most abundant epigenetic modification, which can regulate various nutrient metabolism. This study aimed to investigate effect of iron deficiency on bile acid metabolism and elucidate its mechanism from the perspective of m6A methylation. Results: Iron deficiency (ID) destroyed liver morphology and ultrastructure in suckling piglet. Notably, ID induced moderate dilation of the endoplasmic reticulum and a reduction in mitochondrial number. At the metabolite level, ID significantly promoted bile acid deposition and reshaped bile acid profile. Specifically, ID decreased contents of GCA, CDCA, and 6-KetoLCA, while increasing levels of THDCA, TωMCA, DCA, GDCA, and TDCA (P < 0.05). At the molecular level, ID upregulated CYP7A1 expression to promoted bile acid deposition. Moreover, ID significantly decreased m6A content, and reduced expression of FTO and YTHDF2 (P < 0.05). M6A-seq data revealed an increase in m6A methylated peaks on CYP7A1 under ID condition. Importantly, RNA immunoprecipitation and stability experiments demonstrated YTHDF2 could bind and decrease stability of CYP7A1 (P < 0.05). Mechanistically, ID reduced YTHDF2 expression, thereby stabilizing CYP7A1 and driving bile acid accumulation. Conclusion: Iron deficiency induced bile acid deposition in an m6A-YTHDF2-CYP7A1 dependent manner, which further causes liver injury.
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Project description:Appropriate number of neurons and glial cells is generated from neural stem cells (NSCs) by the regulation of cell cycle exit and subsequent differentiation. Although the regulatory mechanism remains obscure, Id (inhibitor of differentiation) proteins are known to contribute critically to NSC proliferation by controlling cell cycle. Here we report that a transcriptional factor, RP58, negatively regulates all 4 Id genes (Id1-Id4) in developing cerebral cortex. Consistently, Rp58 knockout (KO) mice demonstrated enhanced astrogenesis accompanied with an excess of NSCs. These phenotypes were mimicked by the overexpression of all Id genes in wild-type cortical progenitors. Furthermore, Rp58 KO phenotypes were rescued by the knockdown of all Id genes in mutant cortical progenitors but not by the knockdown of each single Id gene. Finally, we determined p57 as an effector gene of RP58-Id-mediated cell fate control. These findings establish RP58 as a novel key regulator that controls the self-renewal and differentiation of NSCs and restriction of astrogenesis by repressing all Id genes during corticogenesis.
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