Embryology

Woolf, Adrian S.; Pitera, Jolanta E.

doi:10.1007/978-3-540-76341-3_1

Cited by 11 publications

(34 citation statements)

References 190 publications

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“…1 A and B). By E13.5, the normal ureteric bud has branched several times ( 21 , 22 ). Whole-mount immunostaining for cytokeratin was undertaken (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The embryonic precursor of the metanephros, which differentiates into the mature mammalian kidney, initiates around the fifth week of human gestation and embryonic day 11 (E11) in mice ( 21 , 22 ). The first phase of its morphogenesis is dominated by epithelial branching, starting with the outgrowth of the ureteric bud from the mesonephric duct, followed by arborization of the bud into the collecting ducts which drain forming urine into the renal pelvis from where it enters the ureter ( 21 ).…”

Section: Introductionmentioning

confidence: 99%

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The planar cell polarity gene Vangl2 is required for mammalian kidney-branching morphogenesis and glomerular maturation

Yates¹,

Papakrivopoulou²,

Long³

et al. 2010

Human Molecular Genetics

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108

157

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The planar cell polarity (PCP) pathway, incorporating non-canonical Wnt signalling, controls embryonic convergent (CE) extension, polarized cell division and ciliary orientation. It also limits diameters of differentiating renal tubules, with mutation of certain components of the pathway causing cystic kidneys. Mutations in mouse Vangl genes encoding core PCP proteins cause neural tube defects (NTDs) and Vangl2 mutations also impair branching of embryonic mouse lung airways. Embryonic metanephric kidneys also undergo branching morphogenesis and Vangl2 is known to be expressed in ureteric bud/collecting duct and metanephric mesenchymal/nephron lineages. These observations led us to investigate metanephroi in Vangl2 mutant mice, Loop-tail (Lp). Although ureteric bud formation is normal in Vangl2Lp/Lp embryos, subsequent in vivo and in vitro branching morphogenesis is impaired. Null mutant kidneys are short, consistent with a CE defect. Differentiating glomerular epithelia express several PCP genes (Vangl1/2, Celsr1, Scrib, Mpk1/2 and Fat4) and glomeruli in Vangl2Lp/Lp fetuses are smaller and contain less prominent capillary loops than wild-type littermates. Furthermore, Vangl2Lp/+ kidneys had modest reduction in glomerular numbers postnatally. Vangl2Lp/Lp metanephroi contained occasional dilated tubules but no overt cystic phenotype. These data show for the first time that a PCP gene is required for normal morphogenesis of both the ureteric bud and metanephric mesenchyme-derived structures. It has long been recognized that certain individuals with NTDs are born with malformed kidneys, and recent studies have discovered VANGL mutations in some NTD patients. On the basis of our mutant mouse study, we suggest that PCP pathway mutations should be sought when NTD and renal malformation co-exist.

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“…1 A and B). By E13.5, the normal ureteric bud has branched several times ( 21 , 22 ). Whole-mount immunostaining for cytokeratin was undertaken (Fig.…”

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The planar cell polarity gene Vangl2 is required for mammalian kidney-branching morphogenesis and glomerular maturation

Yates¹,

Papakrivopoulou²,

Long³

et al. 2010

Human Molecular Genetics

Self Cite

108

157

View full text Add to dashboard Cite

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“…The development of the mammalian kidney during embryonic life is a multi-stage process that derives from reciprocally inductive events between two intermediate mesenchymal progenitors: the ureteric bud (UB) and the metanephric mesenchyme (MM). It begins at E10.5–E11 in the mouse and at 35–37 days of gestation in humans with the induction of the ureteric bud from the nephric duct, followed by mesenchymal to epithelial transition (MET) and branching morphogenesis, and terminates with nephron patterning and elongation (which include proximal and distal tubule morphogenesis and glomerulogenesis) [ 1 , 12 , 30 , 31 , 32 , 33 , 34 , 35 ]. These embryologic events require a tight regulation at the DNA level (mediated by transcriptional factors) and the post-transcriptional level [ 36 ].…”

Section: Pathogenesismentioning

confidence: 99%

Genetics of Congenital Anomalies of the Kidney and Urinary Tract: The Current State of Play

Capone

Morello

Taroni

et al. 2017

IJMS

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Congenital anomalies of the kidney and urinary tract (CAKUT) are the most frequent form of malformation at birth and represent the cause of 40–50% of pediatric and 7% of adult end-stage renal disease worldwide. The pathogenesis of CAKUT is based on the disturbance of normal nephrogenesis, secondary to environmental and genetic causes. Often CAKUT is the first clinical manifestation of a complex systemic disease, so an early molecular diagnosis can help the physician identify other subtle clinical manifestations, significantly affecting the management and prognosis of patients. The number of sporadic CAKUT cases explained by highly penetrant mutations in a single gene may have been overestimated over the years and a genetic diagnosis is missed in most cases, hence the importance of identifying new genetic approaches which can help unraveling the vast majority of unexplained CAKUT cases. The aim of our review is to clarify the current state of play and the future perspectives of the genetic bases of CAKUT.

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“…2B). Similar to the metanephros, the mammalian mesonephros has nephrons containing vascularized glomeruli connected to proximal and distal tubules that empty directly into the ND (Woolf, 2009;Vetter and Gibley, 1966). Indeed, the temporal and spatial gene expression seen in the nephrons of the mesonephros is very similar to that seen in the metanephros .…”

Section: Kidney Morphogenesis In Mammalsmentioning

confidence: 99%

The origin of the mammalian kidney: implications for recreating the kidney in vitro

2015

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The mammalian kidney, the metanephros, is a mesodermal organ classically regarded as arising from the intermediate mesoderm (IM). Indeed, both the ureteric bud (UB), which gives rise to the ureter and the collecting ducts, and the metanephric mesenchyme (MM), which forms the rest of the kidney, derive from the IM. Based on an understanding of the signalling molecules crucial for IM patterning and kidney morphogenesis, several studies have now generated UB or MM, or both, in vitro via the directed differentiation of human pluripotent stem cells. Although these results support the IM origin of the UB and the MM, they challenge the simplistic view of a common progenitor for these two populations, prompting a reanalysis of early patterning events within the IM. Here, we review our understanding of the origin of the UB and the MM in mouse, and discuss how this impacts on kidney regeneration strategies and furthers our understanding of human development.

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Embryology

Cited by 11 publications

References 190 publications

The planar cell polarity gene Vangl2 is required for mammalian kidney-branching morphogenesis and glomerular maturation

The planar cell polarity gene Vangl2 is required for mammalian kidney-branching morphogenesis and glomerular maturation

Genetics of Congenital Anomalies of the Kidney and Urinary Tract: The Current State of Play

The origin of the mammalian kidney: implications for recreating the kidney in vitro

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