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COP5/HKR1改变莱茵衣藻趋化作用期间的纤毛摆动模式并使细胞转向产生偏向。

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

作者信息

Strain Alexis, Kratzberg Nathan, Vu Dan, Miller Emmaline, Wakabayashi Ken-Ichi, Melvin Adam, Kato Naohiro

机构信息

Department of Biological Sciences, Louisiana State University, Baton Rouge, LA, 70803, USA.

Cain Department of Chemical Engineering, Louisiana State University, Baton Rouge, LA, 70803, USA.

出版信息

Sci Rep. 2024 Dec 5;14(1):30354. doi: 10.1038/s41598-024-81455-2.

DOI:10.1038/s41598-024-81455-2
PMID:39639079
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11621555/
Abstract

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.

摘要

本研究调查了模式纤毛虫微藻莱茵衣藻在铵离子趋化过程中纤毛摆动模式的控制。对具有纤毛缺陷的突变株的趋化反应进行筛选发现,缺乏电压门控钙通道α亚基CAV2的菌株在铵离子趋化方面存在缺陷。CAV2调节纤毛摆动模式从不对称波形向对称波形的转变。缺乏COP5/HKR1(衣藻视蛋白5/组氨酸激酶视紫红质1)的菌株在铵离子趋化方面也存在缺陷。相反,在趋光性方面有缺陷的菌株在铵离子趋化方面表现正常。细胞运动分析表明,野生型细胞在沿铵离子梯度向上游动时,会减少纤毛摆动模式从不对称波形向对称波形转变的发生率。相比之下,COP5/HKR1基因敲除菌株在梯度中不会偏向纤毛摆动模式的转变。这一发现表明,COP5/HKR1在衣藻趋化信号转导中起着关键作用,类似于动物的趋化作用。另一方面,纤毛摆动模式的转变会导致随机的方向变化,类似于细菌和古菌的“跑-停”趋化运动。这项研究表明,衣藻的信号转导类似于真核生物的机制,但其细胞运动遵循细菌和古菌的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/11621555/c6807db9926e/41598_2024_81455_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/11621555/faebd37bec19/41598_2024_81455_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/11621555/825f6d562b65/41598_2024_81455_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/11621555/1d5a4639e81f/41598_2024_81455_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/11621555/0de4302f9ccd/41598_2024_81455_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/11621555/ab60a463a7e2/41598_2024_81455_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/11621555/c6807db9926e/41598_2024_81455_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/11621555/faebd37bec19/41598_2024_81455_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/11621555/825f6d562b65/41598_2024_81455_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/11621555/1d5a4639e81f/41598_2024_81455_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/11621555/0de4302f9ccd/41598_2024_81455_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/11621555/ab60a463a7e2/41598_2024_81455_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/11621555/c6807db9926e/41598_2024_81455_Fig6_HTML.jpg

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本文引用的文献

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