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Calmodulin-dependent Signaling

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...

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In Vivo Calcium Imaging in C. elegans Body Wall Muscles

In Vivo Calcium Imaging in C. elegans Body Wall Muscles

Published on: October 20, 2019

Human calmodulin mutations cause arrhythmia and affect neuronal function in C. elegans.

Helene H Jensen¹, Magnus T Frantzen¹, Jonas L Wesseltoft¹

¹Department of Chemistry and Bioscience, Aalborg University, Aalborg Ø 9220, Denmark.

Human Molecular Genetics

|March 15, 2023

Summary

Human calmodulin mutations linked to cardiac arrhythmia also disrupt rhythmic behaviors and neuronal function in the C. elegans model. This study reveals diverse mechanisms underlying these effects, suggesting potential links to neurological diseases.

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In vivo Neuronal Calcium Imaging in C. elegans

In vivo Neuronal Calcium Imaging in C. elegans

Published on: April 10, 2013

Area of Science:

Molecular Biology
Neuroscience
Cardiology

Background:

Mutations in calmodulin are known to cause cardiac arrhythmia in humans by disrupting calcium channel regulation.
Calmodulin's widespread expression and interaction with numerous proteins suggest potential unstudied effects beyond cardiac function.

Purpose of the Study:

To investigate the broader physiological and neurological effects of human calmodulin mutations using the nematode C. elegans as an in vivo model.
To explore how different calmodulin mutations impact calcium binding and downstream cellular functions.

Main Methods:

Utilized the nematode C. elegans to model three human calmodulin mutations with varying calcium-binding impairments.
Assessed the effects of these mutations on rhythmic behaviors (pharynx pumping, defecation) and neuronal functions (neuromuscular junction signaling, chemosensing).

Main Results:

Calmodulin mutations N54I and D96V disrupted rhythmic behaviors in C. elegans, mirroring cardiac effects.
These mutations differentially affected neuronal function: D96V sensitized neuromuscular junction signaling, while N54I had a protective effect.
Mutation N98S did not impact rhythmic behaviors but impaired chemosensing.

Conclusions:

Pathogenic calmodulin mutations exert distinct mechanisms on rhythmic behavior and neuronal function in C. elegans.
The findings support the hypothesis that human calmodulin mutations may contribute to neurological disorders in addition to cardiac conditions.