Welcome to an introductory video tutorial on the External Coincidence Model of photoperiodic flowering.
This tutorial was narrated and produced
by Jay Dandekar and Clara Oh under the guidance of Dr Katia Bonaldi and Dr Susan Golden.
Thanks to their biological clocks, plants make complex calculations
using information from the environment to orchestrate many physiological processes,
such as: Flowering, Plant growth, Pathogen defense, and Gene expression.
This clock regulation allows plants to
provide physiological responses that are appropriate, either to:
a specific time of day, such as the stomata opening that occurs every day at dawn,
or a specific season like flowering, which only occurs during long days in
the model plant Arabidopsis thaliana.
The change in daylight length at a specific location throughout the year, also called photoperiod,
is entirely predictable from one year to another. In fact, it is so predictable that plants
rely on this signal to keep track of the seasons and to flower at the right time,
a phenomenon called photoperiodic flowering.
For a broader introduction to photoperiodic flowering, please refer to the previous tutorial.
After decades of experiments,
a sophisticated model explaining how the long day plant Arabidopsis thaliana
controls flowering has been described. This is called the external coincidence model.
According to this model, two signals are required for flowering.
One is internal to the plant - this is a molecular signal provided by the circadian clock.
The other is external to the plant and is triggered by sunlight.
For flowering to occur, both signals need to coincide. For Arabidopsis, this can
only happen during the summer, when the daytime is longer than night time.
Now, let's dig into the molecular aspects of photoperiodic flowering in Arabidopsis.
Flowering Locust T, or FT is the key signal protein required for flowering.
When FT molecules accumulate up to a certain threshold, they trigger flowering.
Induction of the FT gene itself is mainly governed by the CONSTANS protein, or CO.
Because it is a positive regulator, when CO proteins accumulate,
the expression of FT is triggered. In turn, the expression of CO is regulated by a
family of proteins called CDFs, which stands for CYCLING DOF FACTORS.
CDFs are negative regulators of CO expression. As their name indicates, CDF protein
abundance cycles, because their expression is regulated by the circadian clock.
In the morning, high CDF concentrations
repress CO expression, resulting in low CO protein levels. However, by the end of
the afternoon, the pool of CDF proteins gets degraded which alleviates the
repression of CO expression and results in high CO protein levels by the end of the day.
Let's go backward in this pathway one more time...
Take a deep breath! We're almost there!
The quantity of CDF protein is regulated by a complex of two proteins: FKF1 and GI.
FKF1 and GI are directly regulated by the clock, which confers a daily
oscillation of the protein quantities. At the end of the day,
FKF1 and GI form a complex that degrades CDF proteins,
thereby facilitating the expression of CO. But, I know what you're thinking.
Why does this scenario not occur during short days? What about the need for coincidence
between the clock and light signaling? What about the external coincidence model?
To understand, let's compare what happens under long day versus short day conditions.
The light signal resets the clock every day,
conferring a 24-hour rhythm no matter the season. But, due to the change
in photoperiod throughout the year, the cycling profiles of protein quantities vary,
in other words, exactly when and how much of each protein is produced varies with the photoperiod.
During a long day, the expression of FKF1
and GI is synchronized, which results in high quantities of the FKF1-GI complex.
But, during a short day, their expression is desynchronized.
Because of the protein ratio is unbalanced, not much of the FKF1-GI complex can form.
On top of that, the complex can only be formed when FKF1 is activated by light...
and more precisely, by blue light, because FKF1 is a blue light receptor.
As a result, during a short day, an insufficient amount of FKF1-GI complex is produced.
The consequence is that CDF proteins undergo less degradation during a short day.
Even so, by the end of a short day, the quantity of CDF protein decreases
due to clock regulation. This daily decrease could potentially allow
substantial amount of CO protein to be formed, like it does during long days.
However, CO also requires light stabilization, which means that,
at the end of short days, CO protein quantity remains low because there's no light to
stabilize the CO protein generated. Ultimately, during short days, not enough
FT is produced to reach the critical threshold, whereas during long days,
the FT protein level builds up, day after day, until it reaches the threshold, above
which flowering is triggered. In summary, three factors contribute to
the high levels of FT protein production during long days. First, the coordinated
expression of FKF1 and GI, thanks to the circadian clock.
Second, FKF1-GI complex stabilization by light. And finally, CO protein stabilization by light.
This whole process occurs in the leaves. Once FT is produced, it travels to the bud,
located in the center of the Arabidopsis rosette. Here, FT triggers the developmental process
that results in the production of flowers.