Abstract
The calcium ion (Ca2+) is a diverse secondary messenger with a near-ubiquitous role in a vast array of cellular processes. Cilia are present on nearly every cell type in either a motile or non-motile form; motile cilia generate fluid flow needed for a variety of biological processes, such as left–right body patterning during development, while non-motile cilia serve as the signaling powerhouses of the cell, with vital singling receptors localized to their ciliary membranes. Much of the research currently available on Ca2+-dependent cellular actions and primary cilia are tissue-specific processes. However, basic stimuli-sensing pathways, such as mechanosensation, chemosensation, and electrical sensation (electrosensation), are complex processes entangled in many intersecting pathways; an overview of proposed functions involving cilia and Ca2+ interplay will be briefly summarized here. Next, we will focus on summarizing the evidence for their interactions in basic cellular activities, including the cell cycle, cell polarity and migration, neuronal pattering, glucose-mediated insulin secretion, biliary regulation, and bone formation. Literature investigating the role of cilia and Ca2+-dependent processes at a single-cellular level appears to be scarce, though overlapping signaling pathways imply that cilia and Ca2+ interact with each other on this level in widespread and varied ways on a perpetual basis. Vastly different cellular functions across many different cell types depend on context-specific Ca2+ and cilia interactions to trigger the correct physiological responses, and abnormalities in these interactions, whether at the tissue or the single-cell level, can result in diseases known as ciliopathies; due to their clinical relevance, pathological alterations of cilia function and Ca2+ signaling will also be briefly touched upon throughout this review.
Highlights
Adaptation has long been thought to be the key evolutionary development required for life to exist
In an effort to confirm this as a role for ciliary polycystins cells lacking cilia but maintaining polycystin expression were tested; the results showed that neither Ca2+ nor NO signals were produced at normal and high flow rates [41]
This revealed that are both ciliary PC-1 and polycystin 2 (PC-2) needed for cilia mechanosensation and mechanotransduction, and that the PC-1/2 complex initiates the signaling cascade needed for Ca2+-dependent NO biosynthesis
Summary
Adaptation has long been thought to be the key evolutionary development required for life to exist. Calcium cations (Ca2+) are one such messenger and are involved in many different cellular processes and translating external stimuli into intracellular signaling cascades, as well as having a near-ubiquitous role in the actions of the diverse cellular processes initiated The success of this complex role may, in part, be due to the heterogenic distribution of Ca2+ in areas called “Ca2+ microdomains” found in resting and stimulated cells [1,2]. Motile cilia possess the dynein motor complexes needed to move, while non-motile ones do not; both house a 25 μm diameter cytoskeletal scaffold known as the axoneme [3], which comprises hundreds of proteins and houses nine peripheral microtubule doublets made up of A and B tubules These tubules surround a varying amount of microtubules which determines a cilium’s structure classification; the presence of two microtubules results in a 9 + 2 pattern classification, while a lack of microtubules results in a 9 + 0 pattern [3]. We aim to touch on findings related to the signal transduction mechanisms in the cilia and Ca2+-dependent biologic processes that may be mediated through ciliary signaling
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
