88 P.A. Sabelli · B.A. Larkins
most likely, repressesCYCB1;2expression in wild-type, endoreduplicating
trichomes. Similarly toCYCB1;2,CYCD3;1is not expressed during normal
trichome development. Its ectopic expression, however, led to multicellular
trichomes, which initiated more frequently in the leaf surface than in wild-
type or inCYCB1;2ectopically expressing plants.
In addition, the multicellular phenotype was greatly enhanced com-
pared toCYCB1;2-expressing trichomes (which averaged two to three cells)
(Schnittger et al. 2002b). Further experiments suggested thatCYCD3;1in-
duced expression ofCYCB1;2,andthatSIMrestrictsCYCD3;1function either
in parallel or downstream. When the CDK inhibitorICK1/KRP1was overex-
pressed in trichomes, it caused inhibition of endoreduplication (an average
of two endoreduplication rounds and ploidy = 9C), with trichome downsizing
and a simplified morphology with fewer branches (Schnittger et al. 2003). Co-
expression experiments indicated thatICK1/KRP1was most likely inhibiting
the G1/S-phase transition by repressingCDKA;1.
Trichome endoreduplication appears controlled by immunophilins. Over-
expression ofFIP37, which interacts with the immunophilin FKBP12, was
shown to greatly stimulate endoreduplication specifically in trichomes, with
ploidies up to 256C and enhanced trichome size and branching (Vespa et al.
2004). However, while a great deal is known about the functions of im-
munophilins in animals and particularly in human immune response, plant
immunophilins are largely uncharacterized, and it is currently unclear how
FIP37 affects the endoreduplication cycle in trichomes.
4
Factors That Affect Endoreduplication
4.1
Genetics
Genetic screens inArabidopsishave identified several mutations that impact
endoreduplication. Mutations affecting the switch from mitosis to endoredu-
plication or the extent of endoreduplication have been best characterized
during the study of trichome development. The results indicate that at least
five distinct pathways, such as patterning, DNA catenation, hormone response,
ubiquitin-mediated proteolysis, and cell death impact the endoreduplication
cell cycle in this system (Hulskamp 2004).SIMappears to function both as
a repressor of mitosis and a stimulator of endoreduplication during the de-
velopment of endoreduplicating trichomes (Walker et al. 2000).SIMinteracts
genetically withCYCB1;2as shown by enhanced multicellular phenotype when
CYCB1;2was expressed in asimmutant background (Schnittger et al. 2002b).
SIMencodes a plant-specific small protein containing a motif for cyclin bind-
ing and a motif found in CKIs, similar to those that interact with both D-type