Enhancement of airway ciliary beating mediated via voltage-gated Ca2+ channels/α7-nicotinic receptors in mice

This study investigates the control of ciliary beat patterns during ammonium chemotaxis in the model ciliate microalga Chlamydomonas reinhardtii. Screening the chemotaxis response of mutant strains with ciliary defects revealed that a strain lacking CAV2, the alpha subunit of the voltage-gated calcium channel, is deficient in ammonium chemotaxis. CAV2 regulates the switching of the ciliary beat pattern from the asymmetric to the symmetric waveform. Strains lacking COP5/HKR1 (chlamyopsin 5/histidine kinase rhodopsin 1) are also deficient in ammonium chemotaxis. Conversely, strains defective in phototaxis perform ammonium chemotaxis normally. Cell motility analysis revealed wild-type cells reduce the incidences of switching the ciliary beat pattern from the asymmetric to symmetric waveform when swimming up the ammonium gradient. In contrast, the COP5/HKR1 disrupted strain does not bias ciliary beat pattern switching in the gradient. This finding reveals that COP5/HKR1 plays a critical role in Chlamydomonas chemotaxis signaling transduction, similarly to animal chemotaxis. On the other hand, ciliary beat pattern switching induces randomized directional changes, analogous to run-and-tumble chemotaxis of bacteria and archaea. This study reveals that Chlamydomonas signaling transduction is similar to the eukaryotic mechanism, yet the cellular locomotion follows the bacteria and archaea mechanism.

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Membrane-bound Guanylyl Cyclase COP5/HKR1 changes ciliary beat pattern and biases cell steering during chemotaxis inChlamydomonas reinhardtii

Strain,

Kratzberg,

et al. 2024

Preprint

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This study investigates the control of ciliary beat patterns during ammonium chemotaxis in the model ciliate microalgaeChlamydomonas reinhardtii. Screening the chemotaxis response of mutant strains with ciliary defects revealed that a strain lacking CAV2, the alpha subunit of the voltage-gated Ca2+channel, is deficient in ammonium chemotaxis. CAV2 regulates the switching of the ciliary beat pattern from the asymmetric to the symmetric waveform. Strains lacking COP5/HKR1 (chlamyopsin 5/histidine kinase rhodopsin 1), a membrane-bound guanylyl cyclase, are also deficient in ammonium chemotaxis. Conversely, strains defective in phototaxis perform ammonium chemotaxis normally. Cell motility analysis revealed wild-type cells reduce the incidences of switching the ciliary beat pattern from the asymmetric to symmetric waveform when swimming up the ammonium gradient. In contrast, the COP5/HKR1 disrupted strain does not bias ciliary beat pattern switching in the gradient. This finding reveals that a membrane-bound guanylyl cyclase plays a critical role inChlamydomonaschemotaxis signaling transduction, similarly to animal chemotaxis. On the other hand, ciliary beat pattern switching induces randomized directional changes, analogous to run-and-tumble chemotaxis of bacteria and archaea. This study reveals thatChlamydomonassignaling transduction is similar to the eukaryotic mechanism, yet the cellular locomotion follows the bacteria and archaea mechanism.

show abstract

Enhancement of airway ciliary beating mediated via voltage-gated Ca2+ channels/α7-nicotinic receptors in mice

Cited by 7 publications

References 49 publications

Ambroxol-enhanced ciliary beating via voltage-gated Ca2+ channels in mouse airway ciliated cells

Ambroxol-enhanced ciliary beating via voltage-gated Ca2+ channels in mouse airway ciliated cells

COP5/HKR1 changes ciliary beat pattern and biases cell steering during chemotaxis in Chlamydomonas reinhardtii

Membrane-bound Guanylyl Cyclase COP5/HKR1 changes ciliary beat pattern and biases cell steering during chemotaxis inChlamydomonas reinhardtii

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