Rab11 is essential to pancreas morphogenesis, lumen formation and endocrine mass

Barlow, Haley R.; Ahuja, Neha; Bierschenk, Tyler; Htike, Yadanar; Fassetta, Luke; Azizoglu, D. Berfin; Flores, Juan; Gao, Nan; O, Sean de la; Sneddon, Julie B.; Marciano, Denise K.; Cleaver, Ondine

doi:10.1016/j.ydbio.2023.05.002

Cited by 5 publications

(2 citation statements)

References 57 publications

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“…For instance, to reveal whether polarization plays a role as an apical determinant and as a precursor to microlumen nucleation, as has been reported in the embryonic pancreas and elsewhere, 9 , 25 future studies on PDAC organoids could focus on the recruitment dynamics of PKC-ζ and of other polarity-associated proteins such as Rab11. 59 …”

Section: Discussionmentioning

confidence: 99%

Coexisting mechanisms of luminogenesis in pancreatic cancer-derived organoids

Randriamanantsoa,

Raich,

Saur

et al. 2024

iScience

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Section: Discussionmentioning

confidence: 99%

Coexisting mechanisms of luminogenesis in pancreatic cancer-derived organoids

Randriamanantsoa,

Raich,

Saur

et al. 2024

iScience

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“…In the developing mouse pancreas, apical restriction of Vangl2 maintains epithelial integrity and survival of progenitor cells through modulating ROCK signaling activity, independent of apical-basal cell polarity 36 . Loss of Rab11a/b in the pancreas leads to highly disorganized epithelial defects due to the mislocalization of apical-basal proteins laminin, Par3, and aPKC, but this study did not examine whether this was due to Vangl mis-localization 37 . Interestingly, Vangl2 has a PCP-independent role in the developing lung mesenchyme during branching morphogenesis 38,39 .…”

Section: Previous Studies In Xenopus Gastrulation and Neural Tube Mor...mentioning

confidence: 96%

Disrupted endosomal trafficking of the Vangl-Celsr polarity complex underlies congenital anomalies in trachea-esophageal morphogenesis

Edwards,

Rankin,

Kashyap

et al. 2023

Preprint

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The developmental basis of esophageal atresia and tracheoesophageal fistulas (EA/TEF), life-threatening congenital anomalies where the embryonic foregut fails to properly separate into trachea and esophagus, is poorly understood. Recent genome sequencing reveals that de novo variants in intracellular trafficking genes are enriched in EA/TEF patients, suggesting that these cellular processes regulate foregut morphogenesis. Here we show that mutation of orthologous genes in Xenopus disrupts trachea-esophageal separation like EA/TEF patients. We identify the underlying mechanism showing that the Rab11a recycling endosome pathway is required to localize Vangl-Celsr polarity complexes at the apical cell surface where opposite sides of the foregut tube fuses forming a transient epithelial bilayer. A partial loss of endosome trafficking or knockdown of the Vangl/Celsr complex disrupts cell polarity and planar cell division. Mutant cells accumulate in the disorganize septum, fail to downregulate cadherin, and do not separate into distinct trachea and esophagus. These data provide new insights into the mechanisms of congenital anomalies and general paradigms of tissue fusion during organogenesis.

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