Suppression of a myosin defect by a kinesin-related gene

Lillie, Sue H.; Brown, Susan S.

doi:10.1038/356358a0

Cited by 201 publications

(151 citation statements)

References 27 publications

Supporting

Mentioning

147

Contrasting

Order By: Relevance

“…SMY1 has been suggested to no longer function as a microtubule-based motor (Lillie and Brown, 1998). Overexpression of SMY1 partially corrects for the defects due to the absence of Myo2p, an S. cerevisiae myosin (Lillie and Brown, 1992). However, this rescue does not depend on microtubules, nor on critical residues in the P-loop of SMY1.…”

Section: Are There Other Kinesins Like Nod?mentioning

confidence: 94%

Orphan Kinesin NOD Lacks Motile Properties But Does Possess a Microtubule-stimulated ATPase Activity

Matthies

Baskin

Hawley

2001

MBoC

View full text Add to dashboard Cite

NOD is a Drosophila chromosome-associated kinesin-like protein that does not fall into the chromokinesin subfamily. Although NOD lacks residues known to be critical for kinesin function, we show that microtubules activate the ATPase activity of NOD Ͼ2000-fold. Biochemical and genetic analysis of two genetically identified mutations of NOD (NOD DTW and NOD "DR2" ) demonstrates that this allosteric activation is critical for the function of NOD in vivo. However, several lines of evidence indicate that this ATPase activity is not coupled to vectorial transport, including 1) NOD does not produce microtubule gliding; and 2) the substitution of a single amino acid in the Drosophila kinesin heavy chain with the analogous amino acid in NOD results in a drastic inhibition of motility. We suggest that the microtubule-activated ATPase activity of NOD provides transient attachments of chromosomes to microtubules rather than producing vectorial transport.

show abstract

Section: Are There Other Kinesins Like Nod?mentioning

confidence: 94%

Orphan Kinesin NOD Lacks Motile Properties But Does Possess a Microtubule-stimulated ATPase Activity

Matthies

Baskin

Hawley

2001

MBoC

View full text Add to dashboard Cite

show abstract

“…There is, however, evidence in yeast that a kinesin-like protein may share function with a myosin. Lillie and Brown (31) reported that the kinesin-like protein, SMY1, can act as a suppressor of a mutation in the MYO2 gene, suggesting that a kinesin-like protein can functionally substitute for a putative actin-based motor.…”

Section: Discussionmentioning

confidence: 99%

Essential role of a kinesin-like protein in Arabidopsis trichome morphogenesis

Oppenheimer

Pollock

Vacik

et al. 1997

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

238

185

View full text Add to dashboard Cite

Little is known about how cell shape is controlled. We are using the morphogenesis of trichomes (plant hairs) on the plant Arabidopsis thaliana as a model to study how cell shape is controlled. Wild-type Arabidopsis trichomes are large, single epidermal cells with a stalk and three or four branches, whereas in zwichel (zwi) mutants the trichomes have a shortened stalk and only two branches. To further understand the role of the ZWI gene in trichome morphogenesis we have cloned the wild-type ZWICHEL (ZWI) gene by T-DNA tagging, and report here that it encodes a member of the kinesin superfamily of microtubule motor proteins. Kinesin proteins transport diverse cellular materials in a directional manner along microtubules. Kinesin-like proteins are characterized by a highly conserved ''head'' region that comprises the motor domain, and a nonconserved ''tail'' region that is thought to participate in recognition and binding of the appropriate cargo.Plant cell expansion is central to plant development. During plant cell differentiation, the relative rates of expansion of different regions of the cell wall determine the final shape of the cell. For most cell types the functional significance of cell shape is evident. For example, the special shape of stomatal guard cells permits the opening and closing of stomata, the shape of spongy mesophyll cells allows for efficient gas exchange, and the broadly expanded but thin shape of leaf epidermal cells increases the surface area of a leaf and allows penetration of light to the underlying photosynthetic mesophyll cells.Plant cell expansion results from a complex interplay of diverse processes. These processes involve the loosening of the cell wall, the maintenance of turgor pressure which is needed to drive cell expansion, and the deposition of new cell wall material (reviewed in refs.

show abstract

“…Mutant alleles of the tub2 gene that impart a specific defect in astral microtubule stability show defects in nuclear migration during mitosis or karyogamy, but have relatively little Recently, five kinesin-like genes, KAR3 (Meluh and Rose, 1990), C1N8 (Hoyt et al, 1992;Roof et al, 1992), KIP1 (Hoyt et al, 1992;Roof et al, 1992) K/P2 (Roof et al, 1992), and SMY1 (Lillie and Brown, 1992), have been identified in budding yeast. Some of these play important roles in spindle function but there is no evidence that their gene products are required for nuclear migration during the mitotic cell cycle.…”

mentioning

confidence: 99%

The JNM1 gene in the yeast Saccharomyces cerevisiae is required for nuclear migration and spindle orientation during the mitotic cell cycle.

McMillan

Tatchell

1994

The Journal of Cell Biology

View full text Add to dashboard Cite

Abstract. JNM1, a novel gene on chromosome XIII in the yeast Saccharomyces cerevisiae, is required for proper nuclear migration, jnml null mutants have a temperature-dependent defect in nuclear migration and an accompanying alteration in astral microtubules. At 30°C, a significant proportion of the mitotic spindles is not properly located at the neck between the mother cell and the bud. This defect is more severe at low temperature. At ll°C, 60% of the cells accumulate with large buds, most of which have two DAPI staining regions in the mother cell. Although mitosis is delayed and nuclear migration is defective in jnml mutants, we rarely observe more than two nuclei in a cell, nor do we frequently observe anuclear cells. No loss of viability is observed at ll°C and cells continue to grow exponentially with increased doubling time. T HE nuclei in the budding yeast Saccharomyces cerevisiae migrate to the neck between the mother cell and the bud prior to mitosis and the spindle microtubules orient along the long axis of the cell. At mitosis the spindle elongates through the neck between the mother cell and the bud and chromosomes separate, depositing one set of chromosomes in the mother cell body and one set in the bud. A key role for microtubules in this process has been shown by the inhibitory effects on nuclear migration by microtubule inhibitors (Jacobs et al., 1988) and by defects in nuclear migration exhibited by some B tubulin mutants (Huffaker et al., 1988). Cytoplasmic (or astral) microtubules appear to be mainly responsible for nuclear migration.Mutant alleles of the tub2 gene that impart a specific defect in astral microtubule stability show defects in nuclear migration during mitosis or karyogamy, but have relatively little

show abstract

Suppression of a myosin defect by a kinesin-related gene

Cited by 201 publications

References 27 publications

Orphan Kinesin NOD Lacks Motile Properties But Does Possess a Microtubule-stimulated ATPase Activity

Orphan Kinesin NOD Lacks Motile Properties But Does Possess a Microtubule-stimulated ATPase Activity

Essential role of a kinesin-like protein in Arabidopsis trichome morphogenesis

The JNM1 gene in the yeast Saccharomyces cerevisiae is required for nuclear migration and spindle orientation during the mitotic cell cycle.

Contact Info

Product

Resources

About