Nature · 2008
Ktu/PF13 is required for cytoplasmic pre-assembly of axonemal dyneins.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Omran Heymut, Kobayashi Daisuke, Olbrich Heike, Tsukahara Tatsuya, Loges Niki T, Hagiwara Haruo, Zhang Qi, Leblond Gerard, O'Toole Eileen, Hara Chikako, Mizuno Hideaki, Kawano Hiroyuki, Fliegauf Manfred, Yagi Toshiki, Koshida Sumito, Miyawaki Atsushi, Zentgraf Hanswalter, Seithe Horst, Reinhardt Richard, Watanabe Yoshinori, Kamiya Ritsu, Mitchell David R, Takeda Hiroyuki
Аннотация
Cilia and flagella are highly conserved organelles that have diverse roles in cell motility and sensing extracellular signals. Motility defects in cilia and flagella often result in primary ciliary dyskinesia. However, the mechanisms underlying cilia formation and function, and in particular the cytoplasmic assembly of dyneins that power ciliary motility, are only poorly understood. Here we report a new gene, kintoun (ktu), involved in this cytoplasmic process. This gene was first identified in a medaka mutant, and found to be mutated in primary ciliary dyskinesia patients from two affected families as well as in the pf13 mutant of Chlamydomonas. In the absence of Ktu/PF13, both outer and inner dynein arms are missing or defective in the axoneme, leading to a loss of motility. Biochemical and immunohistochemical studies show that Ktu/PF13 is one of the long-sought proteins involved in pre-assembly of dynein arm complexes in the cytoplasm before intraflagellar transport loads them for the ciliary compartment.