Lissencephaly-1 promotes the recruitment of dynein and dynactin to transported mRNAs

Dix, Carly I; Soundararajan, HC; Dzhindzhev, NS; Begum, F; Suter, Beat; Ohkura, H; Stephens, E; Bullock, SL (2013). Lissencephaly-1 promotes the recruitment of dynein and dynactin to transported mRNAs. Journal of cell biology, 202(3), pp. 479-494. Rockefeller Institute Press 10.1083/jcb.201211052

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Microtubule-based transport mediates the sorting and dispersal of many cellular components and pathogens. However, the mechanisms by which motor complexes are recruited to and regulated on different cargos remain poorly understood. Here we describe a large-scale biochemical screen for novel factors associated with RNA localization signals mediating minus end-directed mRNA transport during Drosophila development. We identified the protein Lissencephaly-1 (Lis1) and found that minus-end travel distances of localizing transcripts are dramatically reduced in lis1 mutant embryos. Surprisingly, given its well-documented role in regulating dynein mechanochemistry, we uncovered an important requirement for Lis1 in promoting the recruitment of dynein and its accessory complex dynactin to RNA localization complexes. Furthermore, we provide evidence that Lis1 levels regulate the overall association of dynein with dynactin. Our data therefore reveal a critical role for Lis1 within the mRNA localization machinery and suggest a model in which Lis1 facilitates motor complex association with cargos by promoting the interaction of dynein with dynactin.

Item Type:

Journal Article (Original Article)

Division/Institute:

08 Faculty of Science > Department of Biology > Institute of Cell Biology > Drosophila
08 Faculty of Science > Department of Biology > Institute of Cell Biology

UniBE Contributor:

Suter, Beat

Subjects:

500 Science > 570 Life sciences; biology

ISSN:

0021-9525

Publisher:

Rockefeller Institute Press

Language:

English

Submitter:

Jacqueline Schmuckli

Date Deposited:

27 Apr 2014 15:47

Last Modified:

26 May 2015 15:21

Publisher DOI:

10.1083/jcb.201211052

Related URLs:

PubMed ID:

23918939

BORIS DOI:

10.7892/boris.51682

URI:

https://boris.unibe.ch/id/eprint/51682

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