A 0.97-W passively Q-switched Tm:YAP laser with a WSe2 saturable absorber

Zhang, Liang; Zhang, Hongda; Sun, Wei; Chi, Jingyuan; Fu, Lijun; Guan, Yanling; Wang, Han; Jiang, Ziqiu; Wang, Xiaodan

doi:10.1117/12.2587133

Cited by 1 publication

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“…Dzip1 (DAZ interacting zinc finger protein 1) and its close paralog Dzip1L have recently been found to play a role in ciliary bud formation in both Drosophila and mammals 24,29,30 . Downstream of Dzip1/1L, Rab8 and Cby (Chibbly)-Fam92 (family with sequence similarity 92) module work together to regulate cilary membrane formation 24,29,31 .…”

Section: Introductionmentioning

confidence: 99%

Cep290 is cooperatively maintained at basal body by Cep131-Cep162 and Cby-Fam92 modules

Wu,

Chen,

Zhang

et al. 2023

Preprint

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Cilia play critical roles in cell signal transduction and organ development. Defects in cilia function result in a variety of genetic disorders. Cep290 is an evolutionarily conserved ciliopathy protein that bridges the ciliary membrane and axoneme at the basal body and plays critical roles in the initiation of ciliogenesis and TZ assembly. How Cep290 is maintained at basal body and whether axonemal and ciliary membrane localized cues converge to determine the localization of Cep290 remain unknown. Here, we report that the Cep131-Cep162 module near the axoneme and the Cby-Fam92 module close to the membrane synergistically control the basal body localization of Cep290 and the subsequent initiation of ciliogenesis. Concurrent deletion of any protein of the Cep131-Cep162 module and of the Cby-Fam92 module leads to a complete loss of Cep290 from basal body and blocks ciliogenesis at its initiation stage. Our results reveal that the first step of ciliogenesis strictly depend on cooperative and retroactive interactions between Cep131-Cep162, Cby-Fam92 and Cep290, which may contribute to the complex pathogenesis of Cep290-related ciliopathies.

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