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Polycystin-2 Mediated Calcium Signalling in the Model for Autosomal Dominant Polycystic Kidney Disease. | LitMetric

Polycystin-2 Mediated Calcium Signalling in the Model for Autosomal Dominant Polycystic Kidney Disease.

Cells

Department of Microbiology, Anatomy, Physiology and Pharmacology, La Trobe University, Bundoora, Melbourne, VIC 3086, Australia.

Published: March 2024

AI Article Synopsis

Article Abstract

Autosomal dominant polycystic kidney disease (ADPKD) occurs when the proteins Polycystin-1 (PC1, ) and Polycystin-2 (PC2, ) contain mutations. PC1 is a large membrane receptor that can interact and form a complex with the calcium-permeable cation channel PC2. This complex localizes to the plasma membrane, primary cilia and ER. Dysregulated calcium signalling and consequential alterations in downstream signalling pathways in ADPKD are linked to cyst formation and expansion; however, it is not completely understood how PC1 and PC2 regulate calcium signalling. We have studied Polycystin-2 mediated calcium signalling in the model organism by overexpressing and knocking down the expression of the endogenous Polycystin-2 homologue, Polycystin-2. Chemoattractant-stimulated cytosolic calcium response magnitudes increased and decreased in overexpression and knockdown strains, respectively, and analysis of the response kinetics indicates that Polycystin-2 is a significant contributor to the control of Ca responses. Furthermore, basal cytosolic calcium levels were reduced in Polycystin-2 knockdown transformants. These alterations in Ca signalling also impacted other downstream Ca-sensitive processes including growth rates, endocytosis, stalk cell differentiation and spore viability, indicating that is a useful model to study Polycystin-2 mediated calcium signalling.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11012017PMC
http://dx.doi.org/10.3390/cells13070610DOI Listing

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