42 A.J. Wright · L.G. Smith
fluorescently labeled MTs were observed in live BY-2 cells. In one study, PPB
MTs labeled at their plus ends with mammalian CLIP170:GFP had a faster
growth rate and an increased catastrophe frequency when compared to simi-
larly labeled interphase cortical MTs (Dhonukshe and Gadella 2003). Another
study using a different fluorescently tagged MT binding protein (MAP4:GFP)
also observed an increase in cortical MT growth rate and catastrophe fre-
quency during preprophase as well as an increase in MT rescue frequency
and a decrease in the shrinkage rate (Vos et al. 2004). These results of both
studies suggest that alterations to MT dynamics during G2 could be a key
force behind PPB formation. In one proposed model, the observed increase in
catastrophe frequency selectively depolymerizes cortical MTs outside of the
PPB zone, increasing the amount of tubulin available for the polymerization
of PPB MTs and promoting the observed increase in growth rate (Dhonukshe
and Gadella 2003). An alternative model proposes that changes in MT dynam-
ics during preprophase actually increase average MT lengths throughout the
cortex, and that MT bundling selectively stabilizes MTs within the PPB zone
(Vos et al. 2004). This model is similar to the proposal for how MTs form
aligned cortical arrays during interphase (Dixit et al. 2006).
Although the factors responsible for spatially restricted alterations to MT
dynamics/stability needed to bring about PPB formation by either mechan-
ism are largely unknown, members of the MAP65 family of MT bundling pro-
teins, which associate with PPBs in preprophase/prophase cells (Smertenko
et al. 2004) may be important for stabilization of PPB MTs.
2.2.2
Insights from Genetic and Pharmacological Perturbations
One advance in our understanding of how MT lengths are regulated dur-
ing PPB formation has come from studies ofArabidopsisMOR1. Cells of
mor1mutants have disorganized interphase MTs, short, disorganized spin-
dles, short phragmoplasts that tend to fragment, and often lack PPBs (Kawa-
mura et al. 2006; Whittington et al. 2001). TheMOR1gene encodes a member
of the well-characterized MAP215 family of MT binding proteins (Whitting-
ton et al. 2001). Alleles that give the previously described phenotypes are
temperature-sensitive point mutations, while lesions expected to result in
a complete loss of function cause sterility due to defects in cytokinesis fol-
lowing pollen mitosis I (Twell et al. 2002). Two different localization patterns
for MOR1 inArabidopsishave been reported. One anti-MOR1 antibody only
recognizes the plus ends of MTs (Twell et al. 2002) while another labels the en-
tire length of MTs (Kawamura et al. 2006). Kawamura et al. suggest that this
discrepancy can be explained if the epitope recognized by the first antibody
is masked everywhere except at the MT plus end. Together, the phenotypic
and protein localization data suggest that MOR1, like its animal homologues,
is required for the formation of long MTs (Whittington et al. 2001; Kawa-