The Minus End-Directed Motor Kar3 Is Required for Coupling Dynamic Microtubule Plus Ends to the Cortical Shmoo Tip in Budding Yeast

Maddox, Paul S.; Stemple, Jennifer; Satterwhite, Lisa L.; Salmon, Edward D.; Bloom, Kerry

doi:10.1016/s0960-9822(03)00547-5

Cited by 68 publications

(90 citation statements)

References 23 publications

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“…The similar kinetochore distribution pattern in cik1 HU and cin8 mutants raises the possibility that the Cik1/Kar3 complex also plays a role in chromosome congression. Indeed, the Cik1/Kar3 complex binds to the end of the microtubule and promotes its depolymerization (Maddox et al 2003;Sproul et al 2005). However, we found that cin8 mutants are not sensitive to HU.…”

Section: Discussioncontrasting

confidence: 44%

The Cik1/Kar3 Motor Complex Is Required for the Proper Kinetochore–Microtubule Interaction After Stressful DNA Replication

et al. 2011

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In budding yeast Saccharomyces cerevisiae, kinetochores are attached by microtubules during most of the cell cycle, but the duplication of centromeric DNA disassembles kinetochores, which results in a brief dissociation of chromosomes from microtubules. Kinetochore assembly is delayed in the presence of hydroxyurea, a DNA synthesis inhibitor, presumably due to the longer time required for centromeric DNA duplication. Some kinetochore mutants are sensitive to stressful DNA replication as these kinetochore proteins become essential for the establishment of the kinetochore-microtubule interaction after treatment with hydroxyurea. To identify more genes required for the efficient kinetochore-microtubule interaction under stressful DNA replication conditions, we carried out a genome-wide screen for yeast mutants sensitive to hydroxyurea. From this screen, cik1 and kar3 mutants were isolated. Kar3 is the minusend-directed motor protein; Cik1 binds to Kar3 and is required for its motor function. After exposure to hydroxyurea, cik1 and kar3 mutant cells exhibit normal DNA synthesis kinetics, but they display a significant anaphase entry delay. Our results indicate that cik1 cells exhibit a defect in the establishment of chromosome bipolar attachment in the presence of hydroxyurea. Since Kar3 has been shown to drive the poleward chromosome movement along microtubules, our data support the possibility that this chromosome movement promotes chromosome bipolar attachment after stressful DNA replication.

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Section: Discussioncontrasting

confidence: 44%

The Cik1/Kar3 Motor Complex Is Required for the Proper Kinetochore–Microtubule Interaction After Stressful DNA Replication

et al. 2011

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“…Additionally, NCD, which shares 42.2% amino acid sequence identity to ATK5 inside the motor domain was identified as an interacting partner with the ϩTIP EB1 in Drosophila S2 cells (Rogers et al, 2004). A fusion between Kar3p and GFP has been shown to localize to plus-ends of astral microtubules in the budding yeast schmoo tip, although in this case the enrichment was greater during microtubule depolymerization (Maddox et al, 2003). Further advances in microscopic imaging and GFP technology may reveal additional Kinesin-14 family members with ϩTIP activity.…”

Section: Minus-end Motors and Plus-end Trackingmentioning

confidence: 99%

A Minus-End–directed Kinesin with Plus-End Tracking Protein Activity Is Involved in Spindle Morphogenesis

Ambrose

Marcus

et al. 2005

MBoC

116

132

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Diverse kinesin motor proteins are involved in spindle function; however, the mechanisms by which they are targeted to specific sites within spindles are not well understood. Here, we show that a fusion between yellow fluorescent protein (YFP) and a minus-end-directed Kinesin-14 (C-terminal family) from Arabidopsis, ATK5, localizes to mitotic spindle midzones and regions rich in growing plus-ends within phragmoplasts. Notably, in Arabidopsis interphase cells, YFP::ATK5 localizes to microtubules with a preferential enrichment at growing plus-ends; indicating ATK5 is a plus-end tracking protein (؉TIP). This ؉TIP activity is conferred by regions outside of the C-terminal motor domain, which reveals the presence of independent plus-end tracking and minus-end motor activities within ATK5. Furthermore, mitotic spindles of atk5 null mutant plants are abnormally broadened. Based on these data, we propose a model in which ATK5 uses plus-end tracking to reach spindle midzones, where it then organizes microtubules via minus-end-directed motor activity. INTRODUCTIONDuring cell division, the proper segregation of genetic material into daughter cells requires the action of the microtubule spindle apparatus and its associated proteins. The spindle consists of two opposing sets of microtubules oriented with the minus-ends at the poles and the plus-ends at the midzone. The midzone represents the region of overlap between the two halves of the spindle, where microtubule plus-ends terminate at chromosomal kinetochores (kinetochore microtubules) or interdigitate in an antiparallel manner with microtubules from the opposite pole (interpolar microtubules). The spindle midzone is the site of force generation during anaphase spindle elongation (Leslie and Pickett-Heaps, 1983;Khodjakov et al., 2004), and in plants it persists through telophase to form the cytokinetic microtubule apparatus, the phragmoplast (Euteneuer et al., 1982).The assembly and functioning of spindles involve the highly orchestrated activities of diverse microtubule motor proteins. Kinesins convert the energy derived from ATP hydrolysis into translational movement along microtubules (Dagenbach and Endow, 2004;Lawrence et al., 2004). Kinesin-14 family members (previously referred to as C-terminal kinesins), such as Ncd from Drosophila and Kar3p from budding yeast, are unique in that they translocate exclusively toward microtubule minus-ends (Walker et al., 1990). Several Kinesin-14 family members contain microtubule binding sites in their tail regions, which specifies the ability to carry microtubules as cargo along other microtubules; in effect, moving microtubules in relation to one another (Walczak et al., 1997;Narasimhulu and Reddy, 1998;Karabay and Walker, 1999;Matuliene et al., 1999). This finding, in conjunction with subcellular localization and loss-of-function studies, has revealed two distinct roles for Kinesin-14s in spindle functioning. The first role is inferred from studies showing that loss or depletion of various Kinesin-14 family members rescues the s...

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“…However, KAR3 when expressed dimerizes with either Cik1 or Vik1, both non-nucleotide binding proteins, to generate two functionally distinct kinesin-14 motors in vivo (3)(4)(5)(6). Kar3Cik1 during mating promotes MT 2 shortening for karyogamy, the nuclear fusion event (3)(4)(5)(6)(7)(8)(9)(10). In contrast, during mitosis Kar3Cik1 cross-links anti-parallel ipMTs (11), and its inward force stabilizes the spindle by counter-balancing the outward forces generated by kinesin-5 Cin8 and Kip1 (11)(12)(13)(14)(15)(16)(17)(18).…”

mentioning

confidence: 99%

Kinesin Kar3Cik1 ATPase Pathway for Microtubule Cross-linking

Chen

Rayment

Gilbert

2011

Journal of Biological Chemistry

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The Minus End-Directed Motor Kar3 Is Required for Coupling Dynamic Microtubule Plus Ends to the Cortical Shmoo Tip in Budding Yeast

Cited by 68 publications

References 23 publications

The Cik1/Kar3 Motor Complex Is Required for the Proper Kinetochore–Microtubule Interaction After Stressful DNA Replication

The Cik1/Kar3 Motor Complex Is Required for the Proper Kinetochore–Microtubule Interaction After Stressful DNA Replication

A Minus-End–directed Kinesin with Plus-End Tracking Protein Activity Is Involved in Spindle Morphogenesis

Kinesin Kar3Cik1 ATPase Pathway for Microtubule Cross-linking

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