92 P.A. Sabelli · B.A. Larkins
Indeed, a convincing demonstration that ploidy directly regulates, and
it is not merely correlated with, body size comes from a recent study of
Caenorhabtis elegans(Lozano et al. 2006). This investigation also identified
CycE activity as a likely effector of endoreduplication-dependent growth.
Early observations suggested that endoreduplication preferentially occurs
in species with a small genome, and it was proposed that it can be viewed as
an evolutionary strategy compensating for the lack of phylogenetic increase
in nuclear DNA (needed to support the development and metabolism of com-
plex organisms) (Nagl 1976; Derocher et al. 1990). However, in spite of the
overwhelming evidence linking endoreduplication to increased cell size, there
are instances in which the two processes can be uncoupled. For example, mi-
sexpression of CDK inhibitors and dominant-negative CDKs inArapidopsis
(Hemerly et al. 1993; De Veylder et al. 2001; Schnittger et al. 2003), tobacco
(Jasinski et al. 2002), and maize (Leiva-Neto et al. 2004) have shown that
changes in ploidy levels may not be reflected by straightforward changes in
cell size. Indeed, organ and body size are often maintained through com-
pensatory mechanisms involving changes in cell size that counteract ploidy
and nuclear changes. In this respect, endoreduplication may be viewed as one
important mechanism by which cell size could be attained within the devel-
opmental constraints set by higher-order control at the organ or body level.
Interestingly, endoreduplication stops well before the differentiation of tri-
chome or epidermal cells that are located on the surface of organs, arguing
that it does play a role in presetting cell size. However, the size of cells that
are deeply embedded in a tissue may be primarily determined by the physical
and developmental constraints from neighboring cells. Thus, it is conceivable
that endoreduplication allows cell size increase, which may or may not occur
depending on the context (Traas et al. 1998). In this context it is important to
keep in mind that plant cells are vacuolated and that there is a notable distinc-
tion between cell growth, as measured by cytoplasmic macromolecular mass,
and cell expansion, which reflects cell volume increase mostly through vacuo-
lation (Sugimoto-Shirasu and Roberts 2003). Thus, regulation of vacuolation
can contribute to cell enlargement in a way that may be largely independent
of endoreduplication.
How does endoreduplication impact cell growth, as defined above? One
long-standing hypothesis involves an increase in gene expression in endo-
reduplicated cells. A twofold mechanism could be envisioned here. First,
endoreduplication generates more gene templates that could support increased
transcription (D’Amato 1984). Second, endoreduplicated cells often contain
more (Fankhauser and Humphrey 1943) or larger (Kowles and Phillips 1988)
nucleoli, potentially leading to higher rates of net protein synthesis through
enhanced RNA synthesis and ribosome biogenesis. Regulation of chromatin
conformation may play an important role in enhancing gene expression during
endoreduplication. During the mitotic cell cycle, chromatin condenses in prep-
aration of mitosis and this temporarily inhibits gene expression. In contrast, in