Biology Reference
In-Depth Information
hornworm
Manduca sexta
as a key determinator for timing of molting and
metamorphosis (
Callier &Nijhout, 2011
), and hypoxia affects TOR activity
(
Wullschleger, Loewith, & Hall, 2006
).
Another interesting possibility for how fat cells might sense size is that
they may monitor endoreplication number. Endoreplicative tissues such
as the fat body rely on polytene replication to increase the size of cells that
are fully differentiated at the end of embryonic development. In the fat body,
dietary amino acids are intimately linked to the endoreplicative machinery,
which means that starvation results in rapid arrest of DNA replication
(
Britton & Edgar, 1998
). However, changing fat body cell size and
endoreplication number via insulin signaling does not affect developmental
timing or systemic growth (
Colombani et al., 2003
), arguing against the
possibility that endoreplication is the key for measuring cell size.
Although previous work shows that insulin regulates ecdysone biosyn-
thesis (
Caldwell et al., 2005; Colombani et al., 2005; Gibbens et al., 2011;
Mirth et al., 2005; Walkiewicz & Stern, 2009
), it is unlikely that insulin
signaling alone generates the series of ecdysone pulses that are produced dur-
ing the third instar (
Warren et al., 2006
). More likely, insulin is part of the
size-sensing system involved in producing the first of three low-level
ecdysone peaks in the third instar that coincides with the critical weight
checkpoint (
Rewitz & O'Connor, 2011
). Passing this first checkpoint,
corresponding to the accumulation of a certain amount of mass and nutri-
ents, could allow the integration of other signals leading to production of
subsequent peaks. Among other checkpoints, one that likely needs to be
satisfied is that the imaginal disks must have developed sufficiently so that
differentiation can take place during metamorphosis.
2.3. Signaling between the neuroendocrine timing system and
a tissue-autonomous size assessment program
It is well known that lesions to imaginal disks, induced by either physical
damage, radiation or genetic manipulation, also delay metamorphosis
(
Bryant & Levinson, 1985; Hussey, Thompson, & Calhoun, 1927; Poodry
& Woods, 1990; Sehnal & Bryant, 1993; Simpson, Berreur, & Berreur-
Bonnenfant, 1980; Simpson & Scheinderman, 1975; Stieper, Kupershtok,
Driscoll, & Shingleton, 2008
). The fact that transplantation of damaged disks
delays metamorphosis suggests that they produce a secreted signal that acts on
the endocrine system to suppress ecdysone release (
Dewes, 1973
). This devel-
opmental delay allows extra time for damaged or growth perturbed disks
to regenerate and reach their target size before metamorphosis. Since these