Characterization of the unconventional myosin VIII in plant cells and its localization at the post‐cytokinetic cell wall

Reichelt, Stefanie; Knight, Alex E.; Hodge, T. P.; Baluška, Frantǐsek; Šamaj, Jozef; Volkmann, Dieter; Kendrick‐Jones, John

doi:10.1046/j.1365-313x.1999.00553.x

Cited by 210 publications

(191 citation statements)

References 58 publications

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“…The use of antibodies with more defined specificity has been realized in only a few studies. Organelle targeting was observed for antibodies raised against a 170-kDa myosin from pollen tubes (15), and Arabidopsis thaliana myosin 1, a class VIII myosin, has been localized to plasmodesmata and maturing cell plates (16)(17). Recent in vitro motility studies of a higher plant myosin XI reveal unique physical properties with very fast movement along F-actin (18).…”

Section: Carola Holweg* and Peter Nickmentioning

confidence: 99%

RETRACTED: Arabidopsis myosin XI mutant is defective in organelle movement and polar auxin transport

Holweg

Nick

2004

Proc. Natl. Acad. Sci. U.S.A.

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Myosins are eukaryotic molecular motors moving along actin filaments. Only a small set of myosin classes is present in plants, in which myosins have been found to play a role in cytoplasmic streaming and chloroplast movement. Whereas most studies have been done on green algae, more recent data suggest a role of higher plant myosin at the postcytokinetic cell wall. Here we characterize a loss-of-function mutation for a myosin of plant-specific class XI and demonstrate myosin functions during plant development in Arabidopsis. T-DNA insertion in MYA2 caused pleiotropic effects, including flower sterility and dwarf growth. Elongation of epidermal cells, such as in hypocotyls and anther filaments, was reduced by up to 50% of normal length. This effect on anther filaments is responsible for flower sterility. In the meristems of root tips, it was evident that cell division was delayed and that cell plates were mislocated. Like zwichel, a kinesin-related mutation causing two-branched trichomes, the mya2 knockout causes branching defects, but here the trichomes remained unbranched. Growth was also impaired in pollen tubes and root hairs, cells that are highly dependent on vesicle transport. A failure in vesicle flow could be directly confirmed, because cytoplasmic streaming of vesicles and, more so, of large endoplasmic reticulum-based organelles was slowed. The defect in vesicle trafficking was accompanied by failures in basipetal auxin transport, measured in stem segments of inflorescences. This result strongly suggests a causal link between auxin-dependent processes and the distribution of vesicles and membrane-bound molecules by plant myosin

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Section: Carola Holweg* and Peter Nickmentioning

confidence: 99%

RETRACTED: Arabidopsis myosin XI mutant is defective in organelle movement and polar auxin transport

Holweg

Nick

2004

Proc. Natl. Acad. Sci. U.S.A.

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“…Reciprocal stimulation between dimerization via the coiled-coil domains of MYA1 and organelle binding was suggested (Li and Nebenfü hr, 2008a). As for myosin VIII, immunostaining studies showed that it localized to the cell periphery at plant-specific structures such as plasmodesmata and cytokinetic cell plates (Reichelt et al, 1999;Baluska et al, 2001). Recent data from our laboratory and from others confirmed the presence of myosin VIII in plasmodesmata (Golomb et al, 2008) and the cell plate (Van Damme et al, 2004) and further provided evidence for its involvement with endocytosis (Golomb et al, 2008;Sattarzadeh et al, 2008) and its colocalization with the ER (Golomb et al, 2008).…”

mentioning

confidence: 70%

“…The ATM1 clone was kindly provided by Dieter Volkmann from the University of Bonn (Reichelt et al, 1999). The fragments were cloned into the plasmid pART7 downstream to eGFP, with a linker of 10 Ala amino acids between the restriction sites KpnI and BamHI, beside myosin fragments XI-A, XI-D, and XI-G, which were cloned between KpnI and XbaI, and XI-H, which was cloned between KpnI and ClaI.…”

Section: Generation Of Iq Tail and Tail Constructsmentioning

confidence: 99%

A Comparative Study of the Involvement of 17 Arabidopsis Myosin Family Members on the Motility of Golgi and Other Organelles

et al. 2009

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Gene families with multiple members are predicted to have individuals with overlapping functions. We examined all of the Arabidopsis (Arabidopsis thaliana) myosin family members for their involvement in Golgi and other organelle motility. Truncated fragments of all 17 annotated Arabidopsis myosins containing either the IQ tail or tail domains only were fused to fluorescent markers and coexpressed with a Golgi marker in two different plants. We tracked and calculated Golgi body displacement rate in the presence of all myosin truncations and found that tail fragments of myosins MYA1, MYA2, XI-C, XI-E, XI-I, and XI-K were the best inhibitors of Golgi body movement in the two plants. Tail fragments of myosins XI-B, XI-F, XI-H, and ATM1 had an inhibitory effect on Golgi bodies only in Nicotiana tabacum, while tail fragments of myosins XI-G and ATM2 had a slight effect on Golgi body motility only in Nicotiana benthamiana. The best myosin inhibitors of Golgi body motility were able to arrest mitochondrial movement too. No exclusive colocalization was found between these myosins and Golgi bodies in our system, although the excess of cytosolic signal observed could mask myosin molecules bound to the surface of the organelle. From the preserved actin filaments found in the presence of enhanced green fluorescent protein fusions of truncated myosins and the motility of myosin punctae, we conclude that global arrest of actomyosin-derived cytoplasmic streaming had not occurred. Taken together, our data suggest that the above myosins are involved, directly or indirectly, in the movement of Golgi and mitochondria in plant cells.The Arabidopsis (Arabidopsis thaliana) myosin gene family contains 17 members: myosin group XI, which includes 13 members (myosins XI-

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“…7). We speculate that the inhibitory mechanism involves interference with class XI myosins; nevertheless, class VIII myosins may also have a role, since they are associated with PD (Reichelt et al, 1999;Volkmann et al, 2003;Golomb et al, 2008). Although specific inhibition of class VIII myosin cargo binding was reported to have no effect on the targeting of the TMV MP to PD (Avisar et al, 2008a), inhibiting the translocation of this myosin class along actin filaments could still lead to hindrance in the cellular pathway that supports the spread of infection.…”

Section: Discussionmentioning

confidence: 95%

Inhibition of Tobacco Mosaic Virus Movement by Expression of an Actin-Binding Protein

et al. 2009

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The tobacco mosaic virus (TMV) movement protein (MP) required for the cell-to-cell spread of viral RNA interacts with the endoplasmic reticulum (ER) as well as with the cytoskeleton during infection. Whereas associations of MP with ER and microtubules have been intensely investigated, research on the role of actin has been rather scarce. We demonstrate that Nicotiana benthamiana plants transgenic for the actin-binding domain 2 of Arabidopsis (Arabidopsis thaliana) fimbrin (AtFIM1) fused to green fluorescent protein (ABD2:GFP) exhibit a dynamic ABD2:GFP-labeled actin cytoskeleton and myosin-dependent Golgi trafficking. These plants also support the movement of TMV. In contrast, both myosin-dependent Golgi trafficking and TMV movement are dominantly inhibited when ABD2:GFP is expressed transiently. Inhibition is mediated through binding of ABD2:GFP to actin filaments, since TMV movement is restored upon disruption of the ABD2:GFP-labeled actin network with latrunculin B. Latrunculin B shows no significant effect on the spread of TMV infection in either wild-type plants or ABD2:GFP transgenic plants under our treatment conditions. We did not observe any binding of MP along the length of actin filaments.Collectively, these observations demonstrate that TMV movement does not require an intact actomyosin system. Nevertheless, actin-binding proteins appear to have the potential to exert control over TMV movement through the inhibition of myosinassociated protein trafficking along the ER membrane.The mechanism by which plant viruses move from cell to cell and systemically to cause systemic infection has been the subject of intense studies (for review, see

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Characterization of the unconventional myosin VIII in plant cells and its localization at the post‐cytokinetic cell wall

Cited by 210 publications

References 58 publications

RETRACTED: Arabidopsis myosin XI mutant is defective in organelle movement and polar auxin transport

RETRACTED: Arabidopsis myosin XI mutant is defective in organelle movement and polar auxin transport

A Comparative Study of the Involvement of 17 Arabidopsis Myosin Family Members on the Motility of Golgi and Other Organelles

Inhibition of Tobacco Mosaic Virus Movement by Expression of an Actin-Binding Protein

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