DYRK2 knockout mice exhibit fetal growth retardation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA611501 | ENA |
REPOSITORIES: ENA
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Project description:We generated DYRK2-deficient mice using the CRISPR/Cas9 genome editing method and demonstrated that loss of DYRK2 gene causes fetal growth retardation and neonatal lethality at birth. Total RNA from DYRK2-/- whole embryo was compared with those of WT mice by microarray.
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Project description:The solute carrier family 7A member 7 gene (SLC7A7) encodes the light chain of the heterodimeric carrier responsible for cationic amino acid (CAA) transport across the basolateral membranes of epithelial cells in intestine and kidney. Mutations affecting SLC7A7 cause lysinuric protein intolerance (LPI), a multiorgan disorder with clinical symptoms that include visceromegaly, growth retardation, osteoporosis, hyperammonemia, and hyperdibasicaminoaciduria. Here, we describe the consequences of inactivating Slc7a7 in a mouse model of LPI. The Slc7a7 mutation was generated by highthroughput retroviral gene-trapping in embryonic stem cells. The Slc7a7-/- mouse displayed intrauterine growth restriction (IUGR), commonly leading to neonatal lethality. After heavy protein ingestion, the surviving adult animals presented metabolic derangement consistent with that observed in human LPI. IUGR was investigated by examining the expression of main factors controlling fetal growth. Insulinlike growth factor 1, the dominant fetal growth regulator in late gestation, was markedly downregulated as demonstrated by quantitative real-time RT-PCR, immunostaining and Western blot analysis in fetal liver. To further explore the pathophysiology of LPI, gene expression profiling analyses were carried out by DNA microarray technology in intestine and liver of adult Slc7a7-/- mice. Significant up-regulation or down-regulation (two-fold or greater) was observed for 488 transcripts in intestine, and for 521 transcripts in liver. The largest category of differentially expressed genes corresponds to those involved in transport according to Gene Ontology classification. This mouse model offers new insights into the pathophysiology of LPI and into mechanisms linking CAA metabolic pathways and growth control. KEYWORDS: cationic amino acid transport; hyperdibasicaminoaciduria; neonatal lethality. Keywords: Disease state analysis
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Project description:ZFP36L2, zinc finger protein 36, C3H type-like 2 (also known as Brf2, Erf2, Tis11D) is a member of the tristetraprolin (TTP; Zfp36) family of tandem CCCH zinc finger proteins that can bind to AU-rich elements (AREs) in the 3'-untranslated region of mRNAs, leading to their deadenylation and subsequent degradation. We have generated Zfp36l2 knockout mice. Knockout mice were born at the expected Mendelian frequency, but within several weeks of birth they died rather suddenly with pallor and frequent intestinal hemorrhage. These mice exhibited pancytopenia, decreased hematopoietic progenitor cells from fetal liver and yolk sac, and ineffective hematopoietic stem cells. Since ZFP26L2 is likely to function as an ARE-containing mRNA destabilizing protein, we were interested in identifying any abnormally stabilized transcripts in fetal livers from the Zfp36l2 knockout mice whose protein product may directly or indirectly affect hematopoietic stem cell function.
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Project description:Paternally expressed 11/Retrotransposon-like 1 (Peg11/Rtl1) knockout (KO) mice exhibited mid to late fetal lethality or late fetal growth retardation associated with frequent neonatal lethality. The lethal phenotype was largely dependent on genetic background and became more severe with each succeeding generation in the course of backcross experiments to C57BL/6 (B6). We previously suggested these lethal and growth phenotypes were due to severe defects in placental fetal capillaries in labyrinth layer. In this study, we reexamined KO fetuses exhibiting mid fetal lethality with internal bleeding. Importantly, basal region of fetal capillary network was specially damaged, therefore, also leading to poor expansion of the labyrinth layer and placental size reduction in later stage. Apparent up-regulation of Guanine nucleotide binding protein, alpha 2 (Gnai2) and decrement of Transmembrane protein 100 (Tmem100), Mesenchyme homeobox 2 (Meox2) and Lymphatic vessel hyaluronan Receptor 1 (LYVE1) expression were observed in earlier stage of placentas even before apparent morphological changes occurred, suggesting that these genes are involved in the maintenance of fetal capillaries associated with Peg11/Rtl1 in development.
2016-10-19 | GSE88891 | GEO
Project description:Paternally expressed 11/Retrotransposon-like 1 (Peg11/Rtl1) knockout (KO) mice exhibited mid to late fetal lethality or late fetal growth retardation associated with frequent neonatal lethality. The lethal phenotype was largely dependent on genetic background and became more severe with each succeeding generation in the course of backcross experiments to C57BL/6 (B6). We previously suggested these lethal and growth phenotypes were due to severe defects in placental fetal capillaries in labyrinth layer. In this study, we reexamined KO fetuses exhibiting mid fetal lethality with internal bleeding. Importantly, basal region of fetal capillary network was specially damaged, therefore, also leading to poor expansion of the labyrinth layer and placental size reduction in later stage. Apparent up-regulation of Guanine nucleotide binding protein, alpha 2 (Gnai2) and decrement of Transmembrane protein 100 (Tmem100), Mesenchyme homeobox 2 (Meox2) and Lymphatic vessel hyaluronan Receptor 1 (LYVE1) expression were observed in earlier stage of placentas even before apparent morphological changes occurred, suggesting that these genes are involved in the maintenance of fetal capillaries associated with Peg11/Rtl1 in development.
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