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Endometrial zinc transporter Slc39a10/Zip10 is indispensable for progesterone responsiveness and successful pregnancy in mice

ABSTRACT: To investigate the molecular mechanism underlying zinc transporter in the endometrium during embryo implantation, we generated mice with uterine-specific deletion of one of zinc transporter, Zip10. We report the sequencing of the uterine transcriptome of control and uterine-specific Zip10-deficient mice at day 4 (1600h) of pregnancy.

ORGANISM(S): Mus musculus

PROVIDER: GSE252322 | GEO | 2025/02/10

REPOSITORIES: GEO

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Endometrial zinc transporter Slc39a10/Zip10 is indispensable for progesterone responsiveness and successful pregnancy in mice

Project description:Endometrial zinc transporter Slc39a10/Zip10 is indispensable for progesterone responsiveness and successful pregnancy in mice

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The zinc transporter ZIP10 regulates epidermal morphogenesis

Project description:We performed an mRNA-sequencing experiment using ZIP10 positive and negative cells isolated from the ventral skins of WT mice and analyzed gene expression profiles of those cells to identify the functional differences between the two cell types.

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Project description:To determine the physiological roles of ZIP10 and zinc in erythroid progenitor cells, Zip10 was depleted via nucleofector-mediated siRNA delivery into cells and cellular zinc was restricted by DTPA treatment. The transcriptome profiles acquired from RNA-seq were compared with those of control cells.

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Gene expression analysis of RNAs isolated from WT and ZIP10-depleted human keratinocytes

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Adaptation of Cupriavidus metallidurans CH34 to toxic zinc concentrations involves an uncharacterized ABC-type transporter

Project description:Cupriavidus metallidurans CH34 is a well-studied metal-resistant β-proteobacterium and contains a battery of genes involved in the resistance and processing of numerous metals. Here, we performed a directed evolution experiment to obtain derivatives adapted to grow in the presence of zinc at concentrations above the minimal inhibitory concentration for the parental strain. Genetic characterization of one derivative, CH34ZnR, which was also more resistant to cadmium, revealed seven mutations, including inactivation of glpR coding for a DeoR-type transcriptional repressor by insertion of IS1088. The latter resulted in the constitutive expression of the neighboring ABC-type transporter. GlpR and the adjacent ABC transporter are highly similar to the glycerol operon regulator and ATP-driven glycerol importer of Rhizobium leguminosarum bv. viciae VF39, respectively. Deletion of glpR or the ABC transporter and complementation of CH34ZnR with the parental glpR gene further demonstrated that loss of GlpR function, with concomitant induction of the adjacent ABC transporter, is pivotal in the observed phenotype. Moreover, addition of glycerol, presumably by glycerol-mediated reduced GlpR activity, also promoted increased zinc and cadmium resistance. Thus, the ABC-type transporter is proposed to be a new adaptation route during exposure to toxic zinc concentrations.

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Pathophysiological Significance of Impaired KAT7-Dependent Histone H3K14 Acetylation During Zinc Deficiency [RNA-seq]

Project description:Zinc is an indispensable micronutrient for optimal physiological functions, and zinc deficiency has been implicated in the pathogenesis of various human diseases. One potential mechanism underlying such pathogenic effects is the alteration of gene expression caused by zinc deficiency; however, the details of this process remain largely unexplored. Here, we show that during zinc deficiency, the histone acetyltransferase KAT7 loses its enzymatic activity, leading to the attenuated acetylation of histone H3 at Lys14 (H3K14ac) at enhancer regions. Physiologically, the decrease in H3K14ac leads to the upregulation of the expression of ZIP10, a plasma membrane-localized zinc transporter, thereby facilitating the import of extracellular zinc to maintain cellular zinc homeostasis. Moreover, prolonged zinc deficiency in mice induced by a zinc-deficient diet or high-fat diet, accompanied by decreased H3K14ac levels in the liver, upregulated the expression of genes associated with intracellular lipid droplet formation, leading to the accumulation of lipids within liver tissue. Our findings demonstrate that cells respond to zinc deficiency by converting it into an epigenetic signal that drives physiological or pathophysiological biological processes.

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Pathophysiological Significance of Impaired KAT7-Dependent Histone H3K14 Acetylation During Zinc Deficiency [ChIP-seq_Hela]

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Pathophysiological Significance of Impaired KAT7-Dependent Histone H3K14 Acetylation During Zinc Deficiency [ChIP-seq_Mice]

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Enterocyte-specific deletion of metal transporter Zip14 (Slc39a14) alters intestinal homeostasis through epigenetic mechanisms

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