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1 ensitivity of SHR movement to treatment with oryzalin.
2 oderate levels of the microtubule inhibitor, oryzalin.
3 hen the microtubules were depolymerized with oryzalin.
4 r sensitivity to depolymerization by cold or oryzalin.
5 ations of the microtubule-destabilizing drug oryzalin.
6 emoved upon depolymerizing microtubules with oryzalin.
7 tivity to the microtubule destabilizing drug oryzalin.
10 roxyurea, whereas it was induced by sucrose, oryzalin, and auxin, thereby revealing expression charac
11 by the antimicrotubule drugs propyzamide and oryzalin, and right skewing is exacerbated by cold treat
12 ith the anti-microtubule drugs, propyzamide, oryzalin, and trifluralin also failed to open under the
14 by short-term treatments with latrunculin B, oryzalin, brefeldin A (BFA) or wortmannin--all of which
15 the controls, was increasingly variable with oryzalin concentration, meaning that microfibril orienta
16 ubule defects, including hypersensitivity to oryzalin, defects in cell division, cortical array organ
17 s of Bos taurus alpha-tubulin indicated that oryzalin did not interact with this site and had a signi
20 oaniline herbicides (such as trifluralin and oryzalin) have been developed for the selective control
24 ce of the microtubule organization inhibitor oryzalin, suggesting a central role for cytoskeleton reo
25 n the growth zone for all treatments, but on oryzalin the distributions became broad, indicating poor
26 subcellular scale, cellulose microfibrils in oryzalin-treated roots were as well aligned as in contro
27 putational studies, a common binding site of oryzalin, trifluralin, and GB-II-5 on apicomplexan and k
29 arkably sensitive to dinitroanilines such as oryzalin, which disrupt plant but not animal microtubule
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