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PMID:17360970

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Citation

Haghnia, M, Cavalli, V, Shah, SB, Schimmelpfeng, K, Brusch, R, Yang, G, Herrera, C, Pilling, A and Goldstein, LS (2007) Dynactin is required for coordinated bidirectional motility, but not for dynein membrane attachment. Mol. Biol. Cell 18:2081-9

Abstract

Transport of cellular and neuronal vesicles, organelles, and other particles along microtubules requires the molecular motor protein dynein (Mallik and Gross, 2004). Critical to dynein function is dynactin, a multiprotein complex commonly thought to be required for dynein attachment to membrane compartments (Karki and Holzbaur, 1999). Recent work also has found that mutations in dynactin can cause the human motor neuron disease amyotrophic lateral sclerosis (Puls et al., 2003). Thus, it is essential to understand the in vivo function of dynactin. To test directly and rigorously the hypothesis that dynactin is required to attach dynein to membranes, we used both a Drosophila mutant and RNA interference to generate organisms and cells lacking the critical dynactin subunit, actin-related protein 1. Contrary to expectation, we found that apparently normal amounts of dynein associate with membrane compartments in the absence of a fully assembled dynactin complex. In addition, anterograde and retrograde organelle movement in dynactin deficient axons was completely disrupted, resulting in substantial changes in vesicle kinematic properties. Although effects on retrograde transport are predicted by the proposed function of dynactin as a regulator of dynein processivity, the additional effects we observed on anterograde transport also suggest potential roles for dynactin in mediating kinesin-driven transport and in coordinating the activity of opposing motors (King and Schroer, 2000).

Links

PubMed PMC1877108 Online version:10.1091/mbc.E06-08-0695

Keywords

Animals; Biological Transport; Cell Membrane/metabolism; Cells, Cultured; Drosophila Proteins/genetics; Drosophila Proteins/metabolism; Drosophila melanogaster; Dyneins/genetics; Dyneins/metabolism; Humans; Microtubule-Associated Proteins/genetics; Microtubule-Associated Proteins/metabolism; Phenotype; Protein Subunits/genetics; Protein Subunits/metabolism; RNA Interference; Recombinant Fusion Proteins/genetics; Recombinant Fusion Proteins/metabolism

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

DROME:ACTZ

involved_in

GO:0019896: axonal transport of mitochondrion

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

DROME:ACTZ

involved_in

GO:0008090: retrograde axonal transport

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

DROME:ACTZ

involved_in

GO:0008089: anterograde axonal transport

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

HUMAN:DCTN1

involved_in

GO:0007399: nervous system development

ECO:0000303: author statement without traceable support used in manual assertion

P

Seeded From UniProt

complete


See also

References

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