A comparative kidney transcriptome analysis of bicarbonate-loaded insrr-null mice
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ABSTRACT:
PROVIDER: PRJNA825580 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18721618.fastq.gz | Fastqsanger.gz | |||
| SRR18721619.fastq.gz | Fastqsanger.gz | |||
| SRR18721620.fastq.gz | Fastqsanger.gz | |||
| SRR18721621.fastq.gz | Fastqsanger.gz | |||
| SRR18721622.fastq.gz | Fastqsanger.gz |
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Project description:The maintenance of physiological pH level is critical for the life of all organisms. Well known, that kidney is key organ for acid-base regulation in vertebrates. Metabolic alkalosis is the most common acid-base disorder in hospitalized patients, particularly in the surgical critical care unit. The receptor tyrosine kinase IRR (insulin receptor-related receptor), a receptor like the insulin receptor, is involved in acid-base regulation by kidney due to its ability to autophosphorylate under alkalization of extracellular medium (pH > 7.9). IRR expressed in only β-intercalated cells. In mice with a knockout of the insrr gene, which encoding IRR, bicarbonate secretion to the urine is impaired. Here for the first time, we present analysis of kidney transcriptomes from wild type and insrr gene knockout mice under basal or bicarbonate-loaded conditions by 250 mM NaHCO3 in drinking water. Analysis of NGS sequencing data revealed changes in the expression of a number of genes in the kidney. Using real-time PCR we confirmed change of expression of the slc51b, slc26a4, rps7, slc5a2, aqp6, plcd1, gapdh, rny3, lypd2, kcnk5, slc6a6 , atp6v1g3 genes in IRR knockout mice. Also, we found that expression of kcnk5 gene is increased in wild type mice after bicarbonate loading but didn’t change in knockout mice. Gene set enrichment between the IRR knockout and wildtype samples identified that knockout causes alterations in expression of genes related mostly to the ATP metabolic and electron transport chain processes. Thus, for the first time, we described some details of the functioning of the IRR in the kidneys.
2022-04-13 | GSE200638 | GEO
Project description:The maintenance of plasma pH is critical for life in all organisms. The kidney plays a critical role in acid-base regulation in vertebrates by controlling the plasma concentration of bicarbonate. The receptor tyrosine kinase IRR (insulin receptor-related receptor) is expressed in renal β-intercalated cells and is involved in alkali sensing due to its ability to autophosphorylate under alkalization of extracellular medium (pH > 7.9). In mice with a knockout of the insrr gene, which encodes for IRR, urinary bicarbonate secretion in response to alkali loading is impaired. The specific regulatory mechanisms in the kidney that are under the control of IRR remain unknown. To address this issue, we analyzed and compared the kidney transcriptomes of wild-type and insrr knockout mice under basal or bicarbonate-loaded conditions. Transcriptomic analyses revealed a differential regulation of a number of genes in the kidney. Using TaqMan real-time PCR, we confirmed different expressions of the slc26a4, rps7, slc5a2, aqp6, plcd1, gapdh, rny3, kcnk5, slc6a6 and atp6v1g3 genes in IRR knockout mice. Also, we found that the expression of the kcnk5 gene is increased in wild-type mice after bicarbonate loading but not in knockout mice. Gene set enrichment analysis between the IRR knockout and wild-type samples identified that insrr knockout causes alterations in expression of genes related mostly to the ATP metabolic and electron transport chain processes.
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Project description:This RNAseq data was generated by comparing kidney tissue from Fnip1 null mice versus Wildtype Mice
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Project description:Transcriptional profiling of Embryonic Day 14.5 mouse kidneys comparing the infuence of gestational high salt stress on gene expression remolding of BdkrB2 receptor null mice with that of BdkrB2 receptor wild type mice. The BdkrB2 receptor has been shown to be playing a role in renal vascular tone, kidney secretion and reabsorption function, normal kidney development, while impaired BdkrB2 receptor in kidney shown being associated with renal agenesis and renal dysplasia. Goal was to determine the effects of BdkrB2 receptor knockout together with gestational high salt stress on renal gene expression pattern. Two-condition experiment, BdkrB2 null mouse kidney vs. BdkrB2 WT mosue kidney with both on gestational high salt stress . Biological replicates: 3 BdkrB2 null/WT replicates, 3 BdkrB2 WT/null replicates, all 6 replicates were duplicated.
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Project description:Loss of Tsc1 in the kidneys gives rise to rapid polycystogenesis and kidney failure due to the hyperactivation of mTOR complex I (mTORC1). One of the major downstream targets of mTORC1 is S6K1, which is responsible for driving many of the effector functions of mTOR. Strikingly, the loss of S6k1 in the context of hyperactivated mTOR is sufficient to reverse the generation of polycystic kidneys. In an effort to uncover novel direct S6k1 substrates involved in the generation of cystic kidneys, we generated Tsc1-null and Tsc1/S6k1-double null murine inner medullary collecting duct (iMCD3) cell lines using CRISPR/Cas9. Using these two cell lines, we conducted a phosphoproteome screen to search for novel candidates. Using a combination of antibody-motif enrichment and metal affinity enrichment, we provide a comprehensive phosphoproteome profile between these two genotypes.
2020-08-11 | PXD014832 | Pride
Project description:Cells sense and adapt to their environment. Parasitic protists for example, such as African trypanosomes, occupy distinct environments in mammalian hosts, and in insect vectors, and adapt energy metabolism and growth accordingly, but the mechanisms involved remain incompletely characterized. Here we describe environmental sensing dependent upon Trypanosoma brucei Quick IQ-motif protein 1 (QIQ1). We use a genome-scale loss-of-function genetic screen to identify knockdowns associated with gain-of-fitness, or a ‘quick’ growth phenotype, in bloodstream-form cells. The dominant hit, QIQ1 (Tb927.8.6870), encodes a flagellum-localized protein with multiple putative calmodulin-binding IQ-motifs. In a competition assay, qiq1-null cells displayed a density-dependent growth advantage, which was abrogated by calcium chelation. When cells were grown at reduced density in blood serum, with a series of supplements, only bicarbonate restored the qiq1-null competitive advantage. Proteomic analysis indicated that QIQ1 increased the expression of carnitine acetyltransferase, suggesting a role in modulating fatty acid metabolism, while expression of a flagellum-localized calmodulin was both QIQ1 and bicarbonate-dependent. We conclude that trypanosomes sense and adapt to distinct environments in a QIQ1-dependent manner. Our findings suggest that QIQ1-signaling facilitates CO2-sensing to optimize utilization of available nutrients via a pathway involving calcium, calmodulin, and carnitine.
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Project description:Cells sense and adapt to their environment. Parasitic protists for example, such as African trypanosomes, occupy distinct environments in mammalian hosts, and in insect vectors, and adapt energy metabolism and growth accordingly, but the mechanisms involved remain incompletely characterized. Here we describe environmental sensing dependent upon Trypanosoma brucei Quick IQ-motif protein 1 (QIQ1). We use a genome-scale loss-of-function genetic screen to identify knockdowns associated with gain-of-fitness, or a ‘quick’ growth phenotype, in bloodstream-form cells. The dominant hit, QIQ1 (Tb927.8.6870), encodes a flagellum-localized protein with multiple putative calmodulin-binding IQ-motifs. In a competition assay, qiq1-null cells displayed a density-dependent growth advantage, which was abrogated by calcium chelation. When cells were grown at reduced density in blood serum, with a series of supplements, only bicarbonate restored the qiq1-null competitive advantage. Proteomic analysis indicated that QIQ1 increased the expression of carnitine acetyltransferase, suggesting a role in modulating fatty acid metabolism, while expression of a flagellum-localized calmodulin was both QIQ1 and bicarbonate-dependent. We conclude that trypanosomes sense and adapt to distinct environments in a QIQ1-dependent manner. Our findings suggest that QIQ1-signaling facilitates CO2-sensing to optimize utilization of available nutrients via a pathway involving calcium, calmodulin, and carnitine.
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Project description:Cells sense and adapt to their environment. Parasitic protists for example, such as African trypanosomes, occupy distinct environments in mammalian hosts, and in insect vectors, and adapt energy metabolism and growth accordingly, but the mechanisms involved remain incompletely characterized. Here we describe environmental sensing dependent upon Trypanosoma brucei Quick IQ-motif protein 1 (QIQ1). We use a genome-scale loss-of-function genetic screen to identify knockdowns associated with gain-of-fitness, or a ‘quick’ growth phenotype, in bloodstream-form cells. The dominant hit, QIQ1 (Tb927.8.6870), encodes a flagellum-localized protein with multiple putative calmodulin-binding IQ-motifs. In a competition assay, qiq1-null cells displayed a density-dependent growth advantage, which was abrogated by calcium chelation. When cells were grown at reduced density in blood serum, with a series of supplements, only bicarbonate restored the qiq1-null competitive advantage. Proteomic analysis indicated that QIQ1 increased the expression of carnitine acetyltransferase, suggesting a role in modulating fatty acid metabolism, while expression of a flagellum-localized calmodulin was both QIQ1 and bicarbonate-dependent. We conclude that trypanosomes sense and adapt to distinct environments in a QIQ1-dependent manner. Our findings suggest that QIQ1-signaling facilitates CO2-sensing to optimize utilization of available nutrients via a pathway involving calcium, calmodulin, and carnitine.
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