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Loss of the canonical spindle orientation function in the Pins/ LGN homolog AGS 3
Author(s) -
Saadaoui Mehdi,
Konno Daijiro,
Loulier Karine,
Goiame Rosette,
Jadhav Vaibhav,
Mapelli Marina,
Matsuzaki Fumio,
Morin Xavier
Publication year - 2017
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201643048
Subject(s) - library science , computer science
In many cell types, mitotic spindle orientation relies on the canonical “ LGN complex” composed of Pins/ LGN , Mud/Nu MA , and Gα i 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 AGS 3. Whereas the role of Pins and LGN in oriented divisions is extensively documented, involvement of AGS 3 remains controversial. Here, we show that AGS 3 is not required for planar divisions of neural progenitors in the mouse neocortex. AGS 3 is not recruited to the cell cortex and does not rescue LGN loss of function. Despite conserved interactions with Nu MA and Gα i in vitro , comparison of LGN and AGS 3 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.