Centrin3 in trypanosomes maintains the stability of a flagellar inner-arm dynein for cell motility

Ying Wei, Huiqing Hu, Zhao-Rong Lun and Ziyin Li ()
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Ying Wei: University of Texas Medical School at Houston
Huiqing Hu: University of Texas Medical School at Houston
Zhao-Rong Lun: Key Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, School of Life Sciences, and Key Laboratory of Tropical Diseases and Control of the Ministry of Education, Zhongshan Medical School, Sun Yat-Sen University
Ziyin Li: University of Texas Medical School at Houston

Nature Communications, 2014, vol. 5, issue 1, 1-11

Abstract: Abstract Centrin is a conserved component of centrioles in animals and basal bodies in flagellated organisms. It also associates with axonemal inner-arm dyneins and regulates cell motility, but the underlying mechanism remains elusive. In Trypanosoma brucei, three of the five centrins associate with the flagellar basal body, but no centrin has been found to regulate flagellar motility. Here we show that TbCentrin3 is a flagellar protein and knockdown of TbCentrin3 compromises cell motility. Tandem affinity purification followed by mass spectrometry identifies an inner-arm dynein, TbIAD5-1, as the TbCentrin3 partner, and knockdown of TbIAD5-1 causes similar cell motility defect. Further, we demonstrate the interdependence of TbCentrin3 and TbIAD5-1 for maintaining a stable complex in the flagellar axoneme. Together, these results identify the essential role of TbCentrin3 in cell motility by maintaining the stability of an inner-arm dynein in the flagellum, which may be shared by all the centrin-containing flagellated and ciliated organisms.

Date: 2014
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DOI: 10.1038/ncomms5060

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