Loss of the canonical spindle orientation function in the Pins/LGN homolog AGS3

Mehdi Saadaoui, Daijiro Konno, Karine Loulier, Rosette Goiame, Vaibhav Jadhav, Marina Mapelli, Fumio Matsuzaki, Xavier Morin

研究成果: ジャーナルへの寄稿学術誌査読

9 被引用数 (Scopus)

抄録

In many cell types, mitotic spindle orientation relies on the canonical “LGN complex” composed of Pins/LGN, Mud/NuMA, and Gαi subunits. Membrane localization of this complex recruits motor force generators that pull on astral microtubules to orient the spindle. Drosophila Pins shares highly conserved functional domains with its two vertebrate homologs LGN and AGS3. Whereas the role of Pins and LGN in oriented divisions is extensively documented, involvement of AGS3 remains controversial. Here, we show that AGS3 is not required for planar divisions of neural progenitors in the mouse neocortex. AGS3 is not recruited to the cell cortex and does not rescue LGN loss of function. Despite conserved interactions with NuMA and Gαi in vitro, comparison of LGN and AGS3 functional domains in vivo reveals unexpected differences in the ability of these interactions to mediate spindle orientation functions. Finally, we find that Drosophila Pins is unable to substitute for LGN loss of function in vertebrates, highlighting that species-specific modulations of the interactions between components of the Pins/LGN complex are crucial in vivo for spindle orientation.

本文言語英語
ページ(範囲)1509-1520
ページ数12
ジャーナルEMBO Reports
18
9
DOI
出版ステータス出版済み - 9月 2017
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 生化学
  • 分子生物学
  • 遺伝学

フィンガープリント

「Loss of the canonical spindle orientation function in the Pins/LGN homolog AGS3」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル