In
Drosophila,
two in
tersec
ting molecular loops cons
ti
tu
te an au
toregula
tory mechanism
tha
t oscilla
tes wi
th a period close
to 24 hr [
1,
2 and
3]. These loops
touch when pro
teins from one loop, PERIOD (PER) and TIMELESS (TIM), repress
the
transcrip
tion of
their paren
t genes,
period (
per) and
timeless (
tim), by blocking posi
tive
transcrip
tion fac
tors from
the o
ther loop. The arrival of PER and TIM in
to
the nucleus of a clock cell marks
the
timing of
this in
terac
tion be
tween
the
two loops [
4];
thus, con
trol of PER:TIM nuclear accumula
tion is a cen
tral componen
t of
the molecular model of clock func
tion [1, 2 and 3]. If a ligh
t pulse occurs early in
the nigh
t as
the he
terodimer accumula
tes in
the nucleus of clock cells, TIM is degraded, PER is des
tabilized, and clock
time is delayed [1, 2 and 3]. Al
terna
tively, if TIM is degraded during
the la
ter par
t of
the nigh
t, af
ter peak accumula
tion, clock
time advances. Curren
t models s
ta
te
tha
t the effec
t of a ligh
t pulse depends on
the s
ta
te of
the PER:TIM oscilla
tion, which
turns on
the changing levels of TIM. However, previous s
tudies have shown
tha
t ligh
t:dark (LD) regimes mimicking seasonal changes cause behavioral adjus
tmen
ts while al
tering clock gene expression [
5 and
6]. This should be reflec
ted in
the adjus
tmen
t of PER and TIM dynamics. We manipula
ted LD cycles
to assess
the effec
ts of al
tered day leng
th on PER and TIM dynamics in clock cells wi
thin
the cen
tral brain as well as ligh
t-induced rese
tting of locomo
tor rhy
thms.