Characterization of splice isoform switching during human kidney development
Wineberg, Y.; Kanter, I.; Ben-Haim, N.; Pode-Shakked, N.; Bucris, E.; Bar-Lev, T. H.; Oriel, S.; Yehuda, Y.; Gershon, R.; Shukrun, R.; Bar-Lev, D. D.; Urbach, A.; Dekel, B.; Kalisky, T.
Show abstract
Nephrons are the functional units of the kidney. During kidney development, cells from the cap mesenchyme - a transient kidney-specific progenitor state - undergo a mesenchymal to epithelial transition (MET) and subsequently differentiate into the various epithelial cell types that create the tubular structures of the nephron. Faults in this transition can lead to a pediatric malignancy of the kidney called Wilms tumor that mimics normal kidney development. While kidney development has been characterized at the gene expression level, a comprehensive characterization of alternative splicing is lacking. We therefore performed RNA sequencing on cell populations representing early, intermediate, and late developmental stages of the human fetal kidney, as well as three blastemal-predominant Wilms tumor patient-derived xenografts. We identified a set of transcripts that are alternatively spliced between the different developmental stages. Moreover, we found that cells from the earliest developmental stage have a mesenchymal splice-isoform profile that is similar to that of blastemal-predominant Wilms tumors. RNA binding motif enrichment analysis suggests that the mRNA binding proteins ESRP1, ESRP2, RBFOX2, and QKI regulate mRNA splice isoform switching during human kidney development. These findings illuminate new molecular mechanisms involved in kidney development and pediatric kidney tumors.\n\nHIGHLIGHTSO_LIDuring fetal kidney development, kidney progenitor cells undergo a mesenchymal to epithelial transition (MET) and subsequently differentiate into the various epithelial cell types that create the tubular structures of the nephron.\nC_LIO_LIRNA sequencing identifies a set of transcripts that undergo splice isoform switching during the mesenchymal to epithelial transition (MET) that occurs in the course of human fetal kidney development.\nC_LIO_LICells in the early stages of kidney development have a mesenchymal splice-isoform profile that is similar to that observed in blastemal-predominant Wilms tumor patient-derived xenografts (WT-PDX) that represent an aggressive subtype of Wilms tumors.\nC_LIO_LIRNA binding motif enrichment analysis indicates that the mRNA binding proteins ESRP1, ESRP2, RBFOX2, and QKI regulate splice isoform switching during human kidney development.\nC_LI
Matching journals
The top 7 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Mice with renal-specific alterations of stem cell-associated signaling develop symptoms of chronic kidney disease but surprisingly no tumors 94%
- Detection of infiltrating fibroblasts by single-cell transcriptomics in human kidney allografts 93%
- Blockade of mTOR ameliorates IgA Nephropathy by correcting CD89 and CD71 dysfunctions in humanized mice 93%
Similar papers in this journal
- Single cell RNA sequencing reveals differential cell cycle activity in key cell populations during nephrogenesis 97%
- Temporal and sex-dependent gene expression patterns in a renal ischemia-reperfusion injury and recovery pig model 94%
- Creation of X-linked Alport Syndrome Rat Model with Col4a5 Deficiency 94%
Similar papers in this journal
- Single-cell RNA sequencing reveals mRNA splice isoform switching during kidney development 98%
- Hnf4a is required for the development of Cdh6-expressing progenitors into proximal tubules in the mouse kidney 94%
- Proximal tubule cells contribute to the thin descending limb of the loop of Henle during mouse kidney development 94%
Similar papers in this journal
- Differentially expressed tRNA-derived fragments in bovine fetuses with assisted reproduction induced congenital overgrowth syndrome 92%
- Identification of characteristic genomic markers in human hepatoma Huh7 and Huh7.5.1-8 cell lines 90%
- Deletion of FUNDC2 and CMC4 on chromosome Xq28 is sufficient to cause hypergonadotropic hypogonadism in men 89%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.