Rab33b-exocyst interaction mediates localized secretion for focal adhesion turnover and cell migration

Bjørnestad, Synne Arstad; Guadagno, Noemi Antonella; Kjos, Ingrid; Progida, Cinzia

doi:10.1016/j.isci.2022.104250

Cited by 4 publications

(3 citation statements)

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“…RAB33B localizes to the medial Golgi apparatus (Zheng et al, 1998;Starr et al, 2010;Pusapati et al, 2012;Morgan et al, 2019), and its depletion using siRNA resulted in a significantly increased number of Golgiassociated vesicles per stack, suggesting a functional role of the protein in vesicle trafficking at the Golgi apparatus level (Starr et al, 2010). RAB33B is also involved in membrane fusion events, e.g., between autophagosomes and lysosomes (Itoh et al, 2008) and in post-Golgi vesicular trafficking to the plasma membrane, and in particular in delivering β1 integrin cargo for the formation of focal cell contacts with the extracellular matrix (Bjornestad et al, 2022). A close paralog of RAB33B is RAB33A; while these two genes appear to co-regulate aspects of CNS development, RAB33A expression seems to be primarily restricted to the CNS while RAB33B is expressed in several tissues (Cheng et al, 2006;Huang et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Insights in Genetics of Common and Rare Diseases: 2022

2024

Frontiers Research Topics

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Frontiers is more than just an open access publisher of scholarly articles: it is a pioneering approach to the world of academia, radically improving the way scholarly research is managed. The grand vision of Frontiers is a world where all people have an equal opportunity to seek, share and generate knowledge. Frontiers provides immediate and permanent online open access to all its publications, but this alone is not enough to realize our grand goals. Frontiers journal seriesThe Frontiers journal series is a multi-tier and interdisciplinary set of openaccess, online journals, promising a paradigm shift from the current review, selection and dissemination processes in academic publishing. All Frontiers journals are driven by researchers for researchers; therefore, they constitute a service to the scholarly community. At the same time, the Frontiers journal series operates on a revolutionary invention, the tiered publishing system, initially addressing specific communities of scholars, and gradually climbing up to broader public understanding, thus serving the interests of the lay society, too. Dedication to qualityEach Frontiers article is a landmark of the highest quality, thanks to genuinely collaborative interactions between authors and review editors, who include some of the world's best academicians. Research must be certified by peers before entering a stream of knowledge that may eventually reach the public -and shape society; therefore, Frontiers only applies the most rigorous and unbiased reviews. Frontiers revolutionizes research publishing by freely delivering the most outstanding research, evaluated with no bias from both the academic and social point of view. By applying the most advanced information technologies, Frontiers is catapulting scholarly publishing into a new generation. What are Frontiers Research Topics?Frontiers Research Topics are very popular trademarks of the Frontiers journals series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area.

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Section: Discussionmentioning

confidence: 99%

Insights in Genetics of Common and Rare Diseases: 2022

2024

Frontiers Research Topics

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“…RAB33B is expressed in human osteoclasts ( Roy and Roux, 2020 ) and in non-osteoclastic cells, it is also involved in autophagosome formation and maturation ( Itoh et al, 2008 ; Itoh et al, 2011 ; Morgan et al, 2019 ). In addition, a recent siRNA screen to identify RAB proteins involved in cell migration, identified RAB33B as a strong candidate in the regulation of focal adhesion dynamics by modulating the delivery of integrins to focal adhesions ( Bjornestad et al, 2022 ). Therefore, RAB33B could be important in numerous aspects of osteoclast biology.…”

Section: Discussionmentioning

confidence: 99%

“…RAB33B localizes to the medial Golgi apparatus ( Zheng et al, 1998 ; Starr et al, 2010 ; Pusapati et al, 2012 ; Morgan et al, 2019 ), and its depletion using siRNA resulted in a significantly increased number of Golgi-associated vesicles per stack, suggesting a functional role of the protein in vesicle trafficking at the Golgi apparatus level ( Starr et al, 2010 ). RAB33B is also involved in membrane fusion events, e.g., between autophagosomes and lysosomes ( Itoh et al, 2008 ) and in post-Golgi vesicular trafficking to the plasma membrane, and in particular in delivering β1 integrin cargo for the formation of focal cell contacts with the extracellular matrix ( Bjornestad et al, 2022 ). A close paralog of RAB33B is RAB33A ; while these two genes appear to co-regulate aspects of CNS development, RAB33A expression seems to be primarily restricted to the CNS while RAB33B is expressed in several tissues ( Cheng et al, 2006 ; Huang et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

A Rab33b missense mouse model for Smith-McCort dysplasia shows bone resorption defects and altered protein glycosylation

et al. 2023

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Smith McCort (SMC) dysplasia is a rare, autosomal recessive, osteochondrodysplasia that can be caused by pathogenic variants in either RAB33B or DYM genes. These genes codes for proteins that are located at the Golgi apparatus and have a role in intracellular vesicle trafficking. We generated mice that carry a Rab33b disease-causing variant, c.136A>C (p.Lys46Gln), which is identical to that of members from a consanguineous family diagnosed with SMC. In male mice at 4 months of age, the Rab33b variant caused a mild increase in trabecular bone thickness in the spine and femur and in femoral mid-shaft cortical thickness with a concomitant reduction of the femoral medullary area, suggesting a bone resorption defect. In spite of the increase in trabecular and cortical thickness, bone histomorphometry showed a 4-fold increase in osteoclast parameters in homozygous Rab33b mice suggesting a putative impairment in osteoclast function, while dynamic parameters of bone formation were similar in mutant versus control mice. Femur biomechanical tests showed an increased in yield load and a progressive elevation, from WT to heterozygote to homozygous mutants, of bone intrinsic properties. These findings suggest an overall impact on bone material properties which may be caused by disturbed protein glycosylation in cells contributing to skeletal formation, supported by the altered and variable pattern of lectin staining in murine and human tissue cultured cells and in liver and bone murine tissues. The mouse model only reproduced some of the features of the human disease and was sex-specific, manifesting in male but not female mice. Our data reveal a potential novel role of RAB33B in osteoclast function and protein glycosylation and their dysregulation in SMC and lay the foundation for future studies.

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