Journal
SCIENCE
Volume 360, Issue 6390, Pages 758-763Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aar2131
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Funding
- NIH NIDDK [R01 DK076077, DK087635, DK105821, DP3 DK108220]
- American Diabetes Association Training [1-17-PDF-036]
- NIH [1U54DK104309-01, 2R01DK073462, UG3 DK114926-01]
- Columbia Precision Medicine Pilot Award
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Our understanding of kidney disease pathogenesis is limited by an incomplete molecular characterization of the cell types responsible for the organ's multiple homeostatic functions. To help fill this knowledge gap, we characterized 57,979 cells from healthy mouse kidneys by using unbiased single-cell RNA sequencing. On the basis of gene expression patterns, we infer that inherited kidney diseases that arise from distinct genetic mutations but share the same phenotypic manifestation originate from the same differentiated cell type. We also found that the collecting duct in kidneys of adult mice generates a spectrum of cell types through a newly identified transitional cell. Computational cell trajectory analysis and in vivo lineage tracing revealed that intercalated cells and principal cells undergo transitions mediated by the Notch signaling pathway. In mouse and human kidney disease, these transitions were shifted toward a principal cell fate and were associated with metabolic acidosis.
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