VANGL2

Last update 08 May 2025

Basic Info

Synonyms

KIAA1215, Loop-tail protein 1 homolog, LPP1

+ [11]

Introduction

Involved in the control of early morphogenesis and patterning of both axial midline structures and the development of neural plate. Plays a role in the regulation of planar cell polarity, particularly in the orientation of stereociliary bundles in the cochlea. Required for polarization and movement of myocardializing cells in the outflow tract and seems to act via RHOA signaling to regulate this process. Required for cell surface localization of FZD3 and FZD6 in the inner ear (By similarity).

100 Clinical Results associated with VANGL2

100 Translational Medicine associated with VANGL2

0 Patents (Medical) associated with VANGL2

487

Literatures (Medical) associated with VANGL2

01 Jul 2025·Developmental Biology

PCP-dependent polarized mechanics in the cortex of individual cells during convergent extension

Article

Author: Alvarado, José ; Weng, Shinuo ; Wallingford, John B ; Devitt, Caitlin C ; Nyaoga, Bill M

Convergent extension (CE) is a key process for tissue elongation during vertebrate development and is driven by polarized cell behaviors. Here, we used a novel image-based technique to investigate the mechanical properties of individual cells undergoing CE. Our results suggest a PCP- and Septin-dependent mechanical gradient, where cortical tension is higher at the anterior face of the cells compared with their posterior face. Disruption of PCP protein Vangl2 or its downstream effector Septin7 eliminates this mechanical polarity. These findings demonstrate a link between actin organization, PCP signaling, and mechanical polarization, providing new avenues into the mechanochemical regulation of cellular behaviors during CE.

01 Jun 2025·Acta Histochemica

The significance of Itga8 and Vangl2 in kidney development: Insights from yotari mice

Article

Author: Katsuyama, Yu ; Filipović, Natalija ; Gelemanović, Andrea ; Vukojević, Katarina ; Kelam, Nela ; Bajt, Patricija ; Racetin, Anita ; Pavlović, Nikola

The permanent kidney develops from the metanephros through the interaction of the ureteric bud (UB) and metanephric mesenchyme (MM). Congenital anomalies of the kidney and urinary tract (CAKUT) are common prenatal diagnoses, and genetic factors play a critical role in their development. This study explores the involvement of Integrin alpha-8 (Itga8) and Van Gogh-like 2 (Vangl2) proteins in kidney development, using the yotari (yot) mouse model, which harbors a mutation in the Dab1 gene, disrupting Reelin signaling. Immunofluorescence was employed to analyze the spatiotemporal expression patterns of these proteins in embryonic and postnatal kidney samples. Our results show that Itga8 and Vangl2 expression is significantly higher in the embryonic kidneys of yot mice than those of wt mice. However, the two groups observed no significant differences in the temporal expression of these proteins in postnatal kidneys. Spatially, Itga8 was most strongly expressed in the metanephric mesenchyme and renal vesicles/immature glomeruli. At the same time, Vangl2 showed the highest expression in the metanephric mesenchyme, renal vesicles/immature glomeruli, and collecting ducts in yot mice. Our findings suggest that the Dab1 mutation disrupts the expression of Itga8 and Vangl2, contributing to kidney developmental defects associated with CAKUT phenotypesThis increased expression suggests a disruption in the normal regulation of these proteins, likely due to the Dab1 mutation, which impairs Reelin signaling. Still, the exact mechanism through which the Reelin/Dab1 pathway influences the expression of examined markers remains to be elucidated. These results offer valuable insights into the factors associated with kidney malformations and suggest potential therapeutic targets for CAKUT abnormalities.

15 Apr 2025·Development

Rac1 and Nectin3 are essential for planar cell polarity-directed axon guidance in the peripheral auditory system

Article

Author: Clancy, Shaylyn ; Sutherland, Ann ; Smith, Margaret ; Eluvathingal Muttikkal, Tess ; Smith, Matthew ; Xie, Nicholas ; Lu, Xiaowei ; Adylkhan, Aray ; Wang, Jasmine ; Wilson, Phillip ; Fateh, Esha ; Hogan, Arielle

ABSTRACTSpiral ganglion neurons (SGNs) carry sound information from the cochlea to the hindbrain, and innervate either inner or outer hair cells. Type II SGNs (SGNIIs) extend peripheral afferents towards outer hair cells, which make a characteristic 90° turn towards the cochlear base and innervate multiple outer hair cells. It has been shown that the planar cell polarity (PCP) pathway acts non-autonomously in the cochlear epithelium to guide SGNII peripheral afferent turning. However, the underlying mechanisms are unknown. Here, we show that PCP signaling regulates junctional localization of the small GTPase Rac1 and the cell adhesion molecule Nectin3 in mouse cochlear supporting cells (SCs), which serve as intermediate targets of SGNII peripheral afferents. Loss of Rac1 or Nectin3 partially phenocopied SGNII peripheral afferent turning defects in Vangl2 mutants. We present evidence that Rac1 plays a non-autonomous role in part by regulating the localization of core PCP proteins Vangl2 and Dvl3 at the SC–SC junctions, while Nectin3 likely serves a cell adhesion function to control SGNII afferent turning. Together, these experiments identify Nectin3 and Rac1 as regulators of PCP-directed SGNII axon guidance in the cochlea.

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VANGL2

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