1. Light regulation of growth
Light as signal about their environment vs light as food
Plants sense
Light quantity
Light quality (colors)
Light duration
Direction it is
coming from
Must have photoreceptors
that sense specific
wavelengths

2. Types of Phytochrome Responses
2 classes based on speed
3 classes based on fluence
Different responses = Different phytochromes

3. Phytochrome
Protein degradation is important for light regulation
Cop mutants are defective in specific types of protein degradation
COP1 helps target transcription factors for degradation
W/O COP1 they act in dark
In light COP1 is exported to cytoplasm so TF can act
Other COPs are
part of protein
deg apparatus
(signalosome)

4. Other Phytochrome Responses
Circadian rhythms: >30% of genes
Once entrained, continue in constant dark or light!
Give plant headstart on photosynthesis, other processes that need gene expression
Or elongate at night!

5. Other Phytochrome Responses
Circadian rhythms: a –ve loop of transcription-translation
Light & TOC1 activate LHY & CCA1 at dawn
LHY & CCA1 repress TOC1 in day, so they decline too
At night TOC1 is activated (not enough LHY & CCA1)

6. Circadian rhythms: a –ve loop of transcription-translation
Light & TOC1 activate LHY & CCA1 at dawn
LHY & CCA1 transcribe PRR7&PRR9, whose proteins block LHY & CCA1 transcription, LHY &CCA1 proteins are degraded
TTLs of the A. thaliana circadian clock. The morning loop (yellow circle) contains the Myb-like transcription factors CCA1 and LHY, which peak in expression early in the subjective day and promote the expression of PRR7 and PRR9, which reciprocally repress CCA1 and LHY expression. CCA1 and LHY protein levels are regulated by E3 ubiquitin ligase-mediated degradation. In the central loop (pink circle), reduction in CCA1 and LHY levels allows expression of TOC1, which peaks in expression in the evening. TOC1 subsequently activates expression of CCA1 and LHY through a hypothetical component ‘X’, possibly involving CHE. CHE binds directly to the CCA1 promoter inhibiting CCA1 expression, CHE expression is in turn inhibited by CCA1 and TOC1 prevents binding of CHE to the CCA1 promoter by a direct protein–protein interaction. The evening loop (blue circle) compromises TOC1 and a hypothetical component ‘Y’, a role which is partly fulfilled by GI. TOC1 represses GI expression, and GI in turn activates TOC1 expression. GI expression is also repressed by CCA1 and LHY. ELF3 and LUX are also components of the evening loop that directly repress PRR7 to prevent expression in the night. Clock components are also subject to significant post-translational modifications (green box). TOC1 protein levels are balanced by the combined effects of degradation by the ZTL–SCF–E3 ubiquitin ligase complex. This degradation is inhibited by GI binding to ZTL, an interaction which is stabilized in blue light, and PRR3, which competes with ZTL for binding to TOC1, an interaction that is enhanced by phosphorylation. Interaction of TOC1 with PRR5 promotes the accumulation of TOC1 in the nucleus. There are several targets for light input to the clock, as indicated in the figure (see key). Other input signals to the clock include temperature cycles and circadian oscillations of cADPR. Physiological outputs include water flux, stomatal aperture, starch accumulation, and degradation rates, leaf movement and [Ca2+]cyt oscillations. Components that have been demonstrated to act on clock function but whose position has not been fully elucidated have been omitted for clarity

7. Circadian rhythms: a –ve loop of transcription-translation
In evening TOC1 activates ELF 3 & LUX, who block PRR7&PRR9 expression
ZTL marks TOC1 for degradation, but in blue light GI binds ZTL & stops this
TTLs of the A. thaliana circadian clock. The morning loop (yellow circle) contains the Myb-like transcription factors CCA1 and LHY, which peak in expression early in the subjective day and promote the expression of PRR7 and PRR9, which reciprocally repress CCA1 and LHY expression. CCA1 and LHY protein levels are regulated by E3 ubiquitin ligase-mediated degradation. In the central loop (pink circle), reduction in CCA1 and LHY levels allows expression of TOC1, which peaks in expression in the evening. TOC1 subsequently activates expression of CCA1 and LHY through a hypothetical component ‘X’, possibly involving CHE. CHE binds directly to the CCA1 promoter inhibiting CCA1 expression, CHE expression is in turn inhibited by CCA1 and TOC1 prevents binding of CHE to the CCA1 promoter by a direct protein–protein interaction. The evening loop (blue circle) compromises TOC1 and a hypothetical component ‘Y’, a role which is partly fulfilled by GI. TOC1 represses GI expression, and GI in turn activates TOC1 expression. GI expression is also repressed by CCA1 and LHY. ELF3 and LUX are also components of the evening loop that directly repress PRR7 to prevent expression in the night. Clock components are also subject to significant post-translational modifications (green box). TOC1 protein levels are balanced by the combined effects of degradation by the ZTL–SCF–E3 ubiquitin ligase complex. This degradation is inhibited by GI binding to ZTL, an interaction which is stabilized in blue light, and PRR3, which competes with ZTL for binding to TOC1, an interaction that is enhanced by phosphorylation. Interaction of TOC1 with PRR5 promotes the accumulation of TOC1 in the nucleus. There are several targets for light input to the clock, as indicated in the figure (see key). Other input signals to the clock include temperature cycles and circadian oscillations of cADPR. Physiological outputs include water flux, stomatal aperture, starch accumulation, and degradation rates, leaf movement and [Ca2+]cyt oscillations. Components that have been demonstrated to act on clock function but whose position has not been fully elucidated have been omitted for clarity

8. ZTL is both a blue-receptor and an E3 ubiquitin-ligase substrate
ZTL marks TOC1 for degradation, but in blue light GI binds ZTL & stops this
ZTL is both a blue-receptor and an
E3 ubiquitin-ligase substrate
Receptor!
GI binds and also protects it from degradation in blue light
TTLs of the A. thaliana circadian clock. The morning loop (yellow circle) contains the Myb-like transcription factors CCA1 and LHY, which peak in expression early in the subjective day and promote the expression of PRR7 and PRR9, which reciprocally repress CCA1 and LHY expression. CCA1 and LHY protein levels are regulated by E3 ubiquitin ligase-mediated degradation. In the central loop (pink circle), reduction in CCA1 and LHY levels allows expression of TOC1, which peaks in expression in the evening. TOC1 subsequently activates expression of CCA1 and LHY through a hypothetical component ‘X’, possibly involving CHE. CHE binds directly to the CCA1 promoter inhibiting CCA1 expression, CHE expression is in turn inhibited by CCA1 and TOC1 prevents binding of CHE to the CCA1 promoter by a direct protein–protein interaction. The evening loop (blue circle) compromises TOC1 and a hypothetical component ‘Y’, a role which is partly fulfilled by GI. TOC1 represses GI expression, and GI in turn activates TOC1 expression. GI expression is also repressed by CCA1 and LHY. ELF3 and LUX are also components of the evening loop that directly repress PRR7 to prevent expression in the night. Clock components are also subject to significant post-translational modifications (green box). TOC1 protein levels are balanced by the combined effects of degradation by the ZTL–SCF–E3 ubiquitin ligase complex. This degradation is inhibited by GI binding to ZTL, an interaction which is stabilized in blue light, and PRR3, which competes with ZTL for binding to TOC1, an interaction that is enhanced by phosphorylation. Interaction of TOC1 with PRR5 promotes the accumulation of TOC1 in the nucleus. There are several targets for light input to the clock, as indicated in the figure (see key). Other input signals to the clock include temperature cycles and circadian oscillations of cADPR. Physiological outputs include water flux, stomatal aperture, starch accumulation, and degradation rates, leaf movement and [Ca2+]cyt oscillations. Components that have been demonstrated to act on clock function but whose position has not been fully elucidated have been omitted for clarity

9. ZTL is both a blue-receptor and an E3 ubiquitin-ligase substrate
ZTL marks TOC1 for degradation, but in blue light GI binds ZTL & stops this
ZTL is both a blue-receptor and an
E3 ubiquitin-ligase substrate
Receptor!
GI binds and also protects it from degradation in blue light
Transcribed at constant rate, but [protein] 3x dusk
TTLs of the A. thaliana circadian clock. The morning loop (yellow circle) contains the Myb-like transcription factors CCA1 and LHY, which peak in expression early in the subjective day and promote the expression of PRR7 and PRR9, which reciprocally repress CCA1 and LHY expression. CCA1 and LHY protein levels are regulated by E3 ubiquitin ligase-mediated degradation. In the central loop (pink circle), reduction in CCA1 and LHY levels allows expression of TOC1, which peaks in expression in the evening. TOC1 subsequently activates expression of CCA1 and LHY through a hypothetical component ‘X’, possibly involving CHE. CHE binds directly to the CCA1 promoter inhibiting CCA1 expression, CHE expression is in turn inhibited by CCA1 and TOC1 prevents binding of CHE to the CCA1 promoter by a direct protein–protein interaction. The evening loop (blue circle) compromises TOC1 and a hypothetical component ‘Y’, a role which is partly fulfilled by GI. TOC1 represses GI expression, and GI in turn activates TOC1 expression. GI expression is also repressed by CCA1 and LHY. ELF3 and LUX are also components of the evening loop that directly repress PRR7 to prevent expression in the night. Clock components are also subject to significant post-translational modifications (green box). TOC1 protein levels are balanced by the combined effects of degradation by the ZTL–SCF–E3 ubiquitin ligase complex. This degradation is inhibited by GI binding to ZTL, an interaction which is stabilized in blue light, and PRR3, which competes with ZTL for binding to TOC1, an interaction that is enhanced by phosphorylation. Interaction of TOC1 with PRR5 promotes the accumulation of TOC1 in the nucleus. There are several targets for light input to the clock, as indicated in the figure (see key). Other input signals to the clock include temperature cycles and circadian oscillations of cADPR. Physiological outputs include water flux, stomatal aperture, starch accumulation, and degradation rates, leaf movement and [Ca2+]cyt oscillations. Components that have been demonstrated to act on clock function but whose position has not been fully elucidated have been omitted for clarity

10. GI binds and also protects it from degradation in blue light
ZTL is both a blue-receptor and an E3 ubiquitin-ligase substrate receptor!
GI binds and also protects it from degradation in blue light
Transcribed at constant rate, but [protein] 3x dusk
In dark GI released, so ZTL
Ubs TOC1 (unless it has Pi)
but also gets degraded
TTLs of the A. thaliana circadian clock. The morning loop (yellow circle) contains the Myb-like transcription factors CCA1 and LHY, which peak in expression early in the subjective day and promote the expression of PRR7 and PRR9, which reciprocally repress CCA1 and LHY expression. CCA1 and LHY protein levels are regulated by E3 ubiquitin ligase-mediated degradation. In the central loop (pink circle), reduction in CCA1 and LHY levels allows expression of TOC1, which peaks in expression in the evening. TOC1 subsequently activates expression of CCA1 and LHY through a hypothetical component ‘X’, possibly involving CHE. CHE binds directly to the CCA1 promoter inhibiting CCA1 expression, CHE expression is in turn inhibited by CCA1 and TOC1 prevents binding of CHE to the CCA1 promoter by a direct protein–protein interaction. The evening loop (blue circle) compromises TOC1 and a hypothetical component ‘Y’, a role which is partly fulfilled by GI. TOC1 represses GI expression, and GI in turn activates TOC1 expression. GI expression is also repressed by CCA1 and LHY. ELF3 and LUX are also components of the evening loop that directly repress PRR7 to prevent expression in the night. Clock components are also subject to significant post-translational modifications (green box). TOC1 protein levels are balanced by the combined effects of degradation by the ZTL–SCF–E3 ubiquitin ligase complex. This degradation is inhibited by GI binding to ZTL, an interaction which is stabilized in blue light, and PRR3, which competes with ZTL for binding to TOC1, an interaction that is enhanced by phosphorylation. Interaction of TOC1 with PRR5 promotes the accumulation of TOC1 in the nucleus. There are several targets for light input to the clock, as indicated in the figure (see key). Other input signals to the clock include temperature cycles and circadian oscillations of cADPR. Physiological outputs include water flux, stomatal aperture, starch accumulation, and degradation rates, leaf movement and [Ca2+]cyt oscillations. Components that have been demonstrated to act on clock function but whose position has not been fully elucidated have been omitted for clarity

11. GI binds and also protects it from degradation in blue light
ZTL is both a blue-receptor and an E3 ubiquitin-ligase substrate receptor!
GI binds and also protects it from degradation in blue light
Transcribed at constant rate, but [protein] 3x dusk
In dark GI released, so ZTL Ubs TOC1 (unless it has Pi)
but also gets degraded
FKF1 is a related blue receptor that controls flowering
TTLs of the A. thaliana circadian clock. The morning loop (yellow circle) contains the Myb-like transcription factors CCA1 and LHY, which peak in expression early in the subjective day and promote the expression of PRR7 and PRR9, which reciprocally repress CCA1 and LHY expression. CCA1 and LHY protein levels are regulated by E3 ubiquitin ligase-mediated degradation. In the central loop (pink circle), reduction in CCA1 and LHY levels allows expression of TOC1, which peaks in expression in the evening. TOC1 subsequently activates expression of CCA1 and LHY through a hypothetical component ‘X’, possibly involving CHE. CHE binds directly to the CCA1 promoter inhibiting CCA1 expression, CHE expression is in turn inhibited by CCA1 and TOC1 prevents binding of CHE to the CCA1 promoter by a direct protein–protein interaction. The evening loop (blue circle) compromises TOC1 and a hypothetical component ‘Y’, a role which is partly fulfilled by GI. TOC1 represses GI expression, and GI in turn activates TOC1 expression. GI expression is also repressed by CCA1 and LHY. ELF3 and LUX are also components of the evening loop that directly repress PRR7 to prevent expression in the night. Clock components are also subject to significant post-translational modifications (green box). TOC1 protein levels are balanced by the combined effects of degradation by the ZTL–SCF–E3 ubiquitin ligase complex. This degradation is inhibited by GI binding to ZTL, an interaction which is stabilized in blue light, and PRR3, which competes with ZTL for binding to TOC1, an interaction that is enhanced by phosphorylation. Interaction of TOC1 with PRR5 promotes the accumulation of TOC1 in the nucleus. There are several targets for light input to the clock, as indicated in the figure (see key). Other input signals to the clock include temperature cycles and circadian oscillations of cADPR. Physiological outputs include water flux, stomatal aperture, starch accumulation, and degradation rates, leaf movement and [Ca2+]cyt oscillations. Components that have been demonstrated to act on clock function but whose position has not been fully elucidated have been omitted for clarity

12. FKF1 is a related blue receptor that controls flowering
CDF1 binds CO promoter & blocks transcription
TTLs of the A. thaliana circadian clock. The morning loop (yellow circle) contains the Myb-like transcription factors CCA1 and LHY, which peak in expression early in the subjective day and promote the expression of PRR7 and PRR9, which reciprocally repress CCA1 and LHY expression. CCA1 and LHY protein levels are regulated by E3 ubiquitin ligase-mediated degradation. In the central loop (pink circle), reduction in CCA1 and LHY levels allows expression of TOC1, which peaks in expression in the evening. TOC1 subsequently activates expression of CCA1 and LHY through a hypothetical component ‘X’, possibly involving CHE. CHE binds directly to the CCA1 promoter inhibiting CCA1 expression, CHE expression is in turn inhibited by CCA1 and TOC1 prevents binding of CHE to the CCA1 promoter by a direct protein–protein interaction. The evening loop (blue circle) compromises TOC1 and a hypothetical component ‘Y’, a role which is partly fulfilled by GI. TOC1 represses GI expression, and GI in turn activates TOC1 expression. GI expression is also repressed by CCA1 and LHY. ELF3 and LUX are also components of the evening loop that directly repress PRR7 to prevent expression in the night. Clock components are also subject to significant post-translational modifications (green box). TOC1 protein levels are balanced by the combined effects of degradation by the ZTL–SCF–E3 ubiquitin ligase complex. This degradation is inhibited by GI binding to ZTL, an interaction which is stabilized in blue light, and PRR3, which competes with ZTL for binding to TOC1, an interaction that is enhanced by phosphorylation. Interaction of TOC1 with PRR5 promotes the accumulation of TOC1 in the nucleus. There are several targets for light input to the clock, as indicated in the figure (see key). Other input signals to the clock include temperature cycles and circadian oscillations of cADPR. Physiological outputs include water flux, stomatal aperture, starch accumulation, and degradation rates, leaf movement and [Ca2+]cyt oscillations. Components that have been demonstrated to act on clock function but whose position has not been fully elucidated have been omitted for clarity

13. FKF1 is a related blue receptor that controls flowering
CDF1 binds CO promoter & blocks transcription
FKF1 absorbs blue photon& binds GI
TTLs of the A. thaliana circadian clock. The morning loop (yellow circle) contains the Myb-like transcription factors CCA1 and LHY, which peak in expression early in the subjective day and promote the expression of PRR7 and PRR9, which reciprocally repress CCA1 and LHY expression. CCA1 and LHY protein levels are regulated by E3 ubiquitin ligase-mediated degradation. In the central loop (pink circle), reduction in CCA1 and LHY levels allows expression of TOC1, which peaks in expression in the evening. TOC1 subsequently activates expression of CCA1 and LHY through a hypothetical component ‘X’, possibly involving CHE. CHE binds directly to the CCA1 promoter inhibiting CCA1 expression, CHE expression is in turn inhibited by CCA1 and TOC1 prevents binding of CHE to the CCA1 promoter by a direct protein–protein interaction. The evening loop (blue circle) compromises TOC1 and a hypothetical component ‘Y’, a role which is partly fulfilled by GI. TOC1 represses GI expression, and GI in turn activates TOC1 expression. GI expression is also repressed by CCA1 and LHY. ELF3 and LUX are also components of the evening loop that directly repress PRR7 to prevent expression in the night. Clock components are also subject to significant post-translational modifications (green box). TOC1 protein levels are balanced by the combined effects of degradation by the ZTL–SCF–E3 ubiquitin ligase complex. This degradation is inhibited by GI binding to ZTL, an interaction which is stabilized in blue light, and PRR3, which competes with ZTL for binding to TOC1, an interaction that is enhanced by phosphorylation. Interaction of TOC1 with PRR5 promotes the accumulation of TOC1 in the nucleus. There are several targets for light input to the clock, as indicated in the figure (see key). Other input signals to the clock include temperature cycles and circadian oscillations of cADPR. Physiological outputs include water flux, stomatal aperture, starch accumulation, and degradation rates, leaf movement and [Ca2+]cyt oscillations. Components that have been demonstrated to act on clock function but whose position has not been fully elucidated have been omitted for clarity

14. FKF1 is a related blue receptor that controls flowering
CDF1 binds CO promoter & blocks transcription
FKF1 absorbs blue photon& binds GI
Complex enters nucleus, finds CDF1 & tags it with Ub
TTLs of the A. thaliana circadian clock. The morning loop (yellow circle) contains the Myb-like transcription factors CCA1 and LHY, which peak in expression early in the subjective day and promote the expression of PRR7 and PRR9, which reciprocally repress CCA1 and LHY expression. CCA1 and LHY protein levels are regulated by E3 ubiquitin ligase-mediated degradation. In the central loop (pink circle), reduction in CCA1 and LHY levels allows expression of TOC1, which peaks in expression in the evening. TOC1 subsequently activates expression of CCA1 and LHY through a hypothetical component ‘X’, possibly involving CHE. CHE binds directly to the CCA1 promoter inhibiting CCA1 expression, CHE expression is in turn inhibited by CCA1 and TOC1 prevents binding of CHE to the CCA1 promoter by a direct protein–protein interaction. The evening loop (blue circle) compromises TOC1 and a hypothetical component ‘Y’, a role which is partly fulfilled by GI. TOC1 represses GI expression, and GI in turn activates TOC1 expression. GI expression is also repressed by CCA1 and LHY. ELF3 and LUX are also components of the evening loop that directly repress PRR7 to prevent expression in the night. Clock components are also subject to significant post-translational modifications (green box). TOC1 protein levels are balanced by the combined effects of degradation by the ZTL–SCF–E3 ubiquitin ligase complex. This degradation is inhibited by GI binding to ZTL, an interaction which is stabilized in blue light, and PRR3, which competes with ZTL for binding to TOC1, an interaction that is enhanced by phosphorylation. Interaction of TOC1 with PRR5 promotes the accumulation of TOC1 in the nucleus. There are several targets for light input to the clock, as indicated in the figure (see key). Other input signals to the clock include temperature cycles and circadian oscillations of cADPR. Physiological outputs include water flux, stomatal aperture, starch accumulation, and degradation rates, leaf movement and [Ca2+]cyt oscillations. Components that have been demonstrated to act on clock function but whose position has not been fully elucidated have been omitted for clarity

15. FKF1 is a related blue receptor that controls flowering
CDF1 binds CO promoter & blocks transcription
FKF1 absorbs blue photon& binds GI
Complex enters nucleus, finds CDF1 & tags it with Ub
CO can now be
transcribed &
induces FT, etc
TTLs of the A. thaliana circadian clock. The morning loop (yellow circle) contains the Myb-like transcription factors CCA1 and LHY, which peak in expression early in the subjective day and promote the expression of PRR7 and PRR9, which reciprocally repress CCA1 and LHY expression. CCA1 and LHY protein levels are regulated by E3 ubiquitin ligase-mediated degradation. In the central loop (pink circle), reduction in CCA1 and LHY levels allows expression of TOC1, which peaks in expression in the evening. TOC1 subsequently activates expression of CCA1 and LHY through a hypothetical component ‘X’, possibly involving CHE. CHE binds directly to the CCA1 promoter inhibiting CCA1 expression, CHE expression is in turn inhibited by CCA1 and TOC1 prevents binding of CHE to the CCA1 promoter by a direct protein–protein interaction. The evening loop (blue circle) compromises TOC1 and a hypothetical component ‘Y’, a role which is partly fulfilled by GI. TOC1 represses GI expression, and GI in turn activates TOC1 expression. GI expression is also repressed by CCA1 and LHY. ELF3 and LUX are also components of the evening loop that directly repress PRR7 to prevent expression in the night. Clock components are also subject to significant post-translational modifications (green box). TOC1 protein levels are balanced by the combined effects of degradation by the ZTL–SCF–E3 ubiquitin ligase complex. This degradation is inhibited by GI binding to ZTL, an interaction which is stabilized in blue light, and PRR3, which competes with ZTL for binding to TOC1, an interaction that is enhanced by phosphorylation. Interaction of TOC1 with PRR5 promotes the accumulation of TOC1 in the nucleus. There are several targets for light input to the clock, as indicated in the figure (see key). Other input signals to the clock include temperature cycles and circadian oscillations of cADPR. Physiological outputs include water flux, stomatal aperture, starch accumulation, and degradation rates, leaf movement and [Ca2+]cyt oscillations. Components that have been demonstrated to act on clock function but whose position has not been fully elucidated have been omitted for clarity

16. Blue Light Responses
Circadian Rhythms

17. Blue Light Responses
Circadian Rhythms
Solar tracking

18. Blue Light Responses
Circadian Rhythms
Solar tracking
Phototropism

19. Blue Light Responses
Circadian Rhythms
Solar tracking
Phototropism
Inhibiting stem elongation

20. Blue Light Responses
Circadian Rhythms
Solar tracking
Phototropism
Inhibiting stem elongation
Chloroplast movement

21. Blue Light Responses
Circadian Rhythms
Solar tracking
Phototropism
Inhibiting stem elongation
Chloroplast movement
Stomatal opening

22. Blue Light Responses
Circadian Rhythms
Solar tracking
Phototropism
Inhibiting stem elongation
Chloroplast movement
Stomatal opening
Gene expression

23. Blue Light Responses
Circadian Rhythms
Solar tracking
Phototropism
Inhibiting stem elongation
Chloroplast movement
Stomatal opening
Gene expression
Flowering in Arabidopsis

24. Blue Light Responses
Circadian Rhythms
Solar tracking
Phototropism
Inhibiting stem elongation
Chloroplast movement
Stomatal opening
Gene expression
Flowering in Arabidopsis
Responses vary in their fluence requirements

25. Blue Light Responses
Circadian Rhythms
Solar tracking
Phototropism
Inhibiting stem elongation
Chloroplast movement
Stomatal opening
Gene expression
Flowering in Arabidopsis
Responses vary in their fluence requirements & lag time

26. Blue Light Responses
Responses vary in their fluence requirements & lag time
Stomatal opening is reversible by green light; others aren’t

27. Blue Light Responses
Responses vary in their fluence requirements & lag time
Stomatal opening is reversible by green light; others aren’t
Multiple blue receptors with
different functions!

28. Blue Light Responses
Responses vary in their fluence requirements & lag time
Stomatal opening is reversible by green light; others aren’t
Multiple blue receptors with
different functions!
Identified genetically

29. Blue Light Responses
Responses vary in their fluence requirements & lag time
Stomatal opening is reversible by green light; others aren’t
Multiple blue receptors with
different functions!
Identified genetically, then clone
the gene and identify the protein

30. Blue Light Responses
Responses vary in their fluence requirements & lag time
Stomatal opening is reversible by green light; others aren’t
Multiple blue receptors with
different functions!
Identified genetically, then clone
the gene and identify the protein
Cryptochromes repress hypocotyl
elongation

31. Blue Light Responses
Identified genetically, then clone the gene and identify the protein
Cryptochromes repress hypocotyl elongation
Stimulate flowering

32. Blue Light Responses
Identified genetically, then clone the gene and identify the protein
Cryptochromes repress hypocotyl elongation
Stimulate flowering
Set the circadian clock (in humans, too!)

33. Blue Light Responses
Identified genetically, then clone the gene and identify the protein
Cryptochromes repress hypocotyl elongation
Stimulate flowering
Set the circadian clock (in humans, too!)
Stimulate anthocyanin synthesis

34. Blue Light Responses
Identified genetically, then clone the gene and identify the protein
Cryptochromes repress hypocotyl elongation
Stimulate flowering
Set the circadian clock (in humans, too!)
Stimulate anthocyanin synthesis
3 CRY genes

35. Blue Light Responses
3 CRY genes
All have same basic structure:
Photolyase-like domain binds FAD and a pterin (MTHF) that absorbs blue & transfers energy to FAD in photolyase
(an enzyme that uses light energy to repair pyr dimers)

36. Blue Light Responses
3 CRY genes
All have same basic structure:
Photolyase-like domain binds FAD and a pterin (MTHF) that absorbs blue & transfers energy to FAD in photolyase
(an enzyme that uses light energy to repair pyr dimers)
DAS binds COP1 & has nuclear localization signals

37. Blue Light Responses
3 CRY genes
All have same basic structure:
Photolyase-like domain binds FAD and a pterin (MTHF) that absorbs blue & transfers energy to FAD in photolyase
(an enzyme that uses light energy to repair pyr dimers)
DAS binds COP1 & has nuclear localization signals
CRY1 & CRY2 kinase proteins after absorbing blue

38. Blue Light Responses
3 CRY genes
CRY1 & CRY2 kinase proteins after absorbing blue
CRY3 repairs mt & cp DNA!

39. Blue Light Responses
3 CRY genes
CRY1 regulates blue effects on growth
Triggers very rapid changes in membrane potential & growth

40. Blue Light Responses
3 CRY genes
CRY1 regulates blue effects on growth
Triggers very rapid changes in membrane potential & growth
Opens anion channels in PM

41. Blue Light Responses
3 CRY genes
CRY1 regulates blue effects on growth: light-stable
Triggers rapid changes in PM potential & growth
Opens anion channels in PM
Stimulates anthocyanin synthesis

42. Blue Light Responses
3 CRY genes
CRY1 regulates blue effects on growth: light-stable
Triggers rapid changes in PM potential & growth
Opens anion channels in PM
Stimulates anthocyanin synthesis
Entrains the circadian clock

43. Blue Light Responses
3 CRY genes
CRY1 regulates blue effects on growth: light-stable
Triggers rapid changes in PM potential & growth
Opens anion channels in PM
Stimulates anthocyanin synthesis
Entrains the circadian clock
Also accumulates in nucleus & interacts with PHY & COP1 to regulate photomorphogenesis, probably by kinasing substrates

44. Blue Light Responses
3 CRY genes
CRY1 regulates blue effects on growth: light-stable
Triggers rapid changes in PM potential & growth
Opens anion channels in PM
Stimulates anthocyanin synthesis
Entrains the circadian clock
Also accumulates in nucleus & interacts with PHY & COP1 to regulate photomorphogenesis, probably by kinasing substrates
2. CRY2 controls flowering

45. Blue Light Responses
3 CRY genes
CRY1 regulates blue effects on growth: light-stable
2. CRY2 controls flowering: little effect on other processes
Light-labile

46. Blue Light Responses
3 CRY genes
CRY1 regulates blue effects on growth
2. CRY2 regulates flowering: little effect on other processes
Light-labile
3. CRY3 enters cp & mito, where binds & repairs DNA

47. Blue Light Responses
3 CRY genes
CRY1 regulates blue effects on growth
2. CRY2 controls flowering: little effect on other processes
CRY3 enters cp & mito, where binds & repairs DNA!
Cryptochromes are not
involved in phototropism or
stomatal opening!

48. Blue Light Responses
Cryptochromes are not involved in phototropism or
stomatal opening!
Phototropins are!

49. Blue Light Responses
Phototropins are involved in phototropism & stomatal opening!
Many names (nph, phot, rpt) since found by several different mutant screens

50. Phototropins
Many names (nph, phot, rpt) since found by several different mutant screens
Mediate blue light-induced growth enhancements

51. Phototropins
Many names (nph, phot, rpt) since found by several different mutant screens
Mediate blue light-induced growth enhancement & blue light-dependent activation of the plasma membrane H+-ATPase in guard cells

52. Phototropins
Many names (nph, phot, rpt) since found by several different mutant screens
Mediate blue light-induced growth enhancement & blue light-dependent activation of the plasma membrane H+-ATPase in guard cells
Contain light-activated serine-threonine kinase domain and LOV1 (light-O2-voltage) and LOV2 repeats

53. Phototropins
Many names (nph, phot, rpt) since found by several different mutant screens
Mediate blue light-induced growth enhancement & blue light-dependent activation of the plasma membrane H+-ATPase in guard cells
Contain light-activated serine-threonine kinase domain and LOV1 (light-O2-voltage) and LOV2 repeats
LOV1 & LOV2 bind FlavinMonoNucleotide cofactors

54. Phototropins
Many names (nph, phot, rpt) since found by several different mutant screens
Mediate blue light-induced growth enhancement & blue light-dependent activation of the plasma membrane H+-ATPase in guard cells
Contain light-activated serine-threonine kinase domain and LOV1 (light-O2-voltage) and LOV2 repeats
LOV1 & LOV2 bind FlavinMonoNucleotide cofactors
After absorbing blue rapidly autophosphorylate & kinase other proteins

55. Phototropins
After absorbing blue rapidly autophosphorylate & kinase other proteins
1 result = phototropism
due to uneven auxin
transport

56. Phototropins
After absorbing blue rapidly autophosphorylate & kinase other proteins
1 result = phototropism
due to uneven auxin
transport
Send more to side away
from light!

57. Phototropins
After absorbing blue rapidly autophosphorylate & kinase other proteins
1 result = phototropism
due to uneven auxin
transport
Send more to side away
from light!
PHOT 1 mediates LF

58. Phototropins
After absorbing blue rapidly autophosphorylate & kinase other proteins
1 result = phototropism
due to uneven auxin
transport
Send more to side away
from light!
PHOT 1 mediates LF
PHOT2 mediates HIR

59. Phototropins
2nd result = stomatal opening via stimulation of guard cell PM proton pump
Also requires photosynthesis by guard cells!

60. Phototropins
2nd result = stomatal opening via stimulation of guard cell PM proton pump
Also requires photosynthesis by guard cells & signaling from xanthophylls

61. Phototropins
2nd result = stomatal opening via stimulation of guard cell PM proton pump
Also requires photosynthesis by guard cells & signaling from xanthophylls
npq mutants don’t
make zeaxanthin &
lack specific blue
response

62. Phototropins
2nd result = stomatal opening via stimulation of guard cell PM proton pump
Also requires photosynthesis by guard cells & signaling from xanthophylls
npq mutants don’t
make zeaxanthin &
lack specific blue
response
Basic idea: open when pump in K+

63. Phototropins
2nd result = stomatal opening via stimulation of guard cell PM proton pump
Also requires photosynthesis by guard cells & signaling from xanthophylls
npq mutants don’t
make zeaxanthin &
lack specific blue
response
Basic idea: open when pump in K+
Close when pump out K+

64. Phototropins
Basic idea: open when pump in K+
Close when pump out K+
Control is hideously complicated!

65. Phototropins
Basic idea: open when pump in K+
Close when pump out K+
Control is hideously complicated!
Mainly controlled by blue light

66. Phototropins
Basic idea: open when pump in K+
Close when pump out K+
Control is hideously complicated!
Mainly controlled by blue light but red also plays role

67. Phototropins
Basic idea: open when pump in K+
Close when pump out K+
Control is hideously complicated!
Mainly controlled by blue light
but red also plays role
Light intensity is also important

68. Phototropins
Mainly controlled by blue light, but red also plays role
Light intensity is also important due to effect on
[photosynthate] in guard cells

69. Phototropins
Mainly controlled by blue light, but red also plays role
Light intensity is also important due to effect on
[photosynthate] in guard cells
PHOT1 &2 also help

70. Phototropins
Mainly controlled by blue light, but red also plays role
Light intensity is also important due to effect on
[photosynthate] in guard cells
PHOT1 &2 also help
Main GC blue
receptor is zeaxanthin!

71. Phototropins
Mainly controlled by blue light, but red also plays role
Light intensity is also important due to effect on
[photosynthate] in guard cells
PHOT1 &2 also help
Main GC blue
receptor is zeaxanthin!
Reason for green reversal

72. Phototropins
Mainly controlled by blue light, but red also plays role
Light intensity is also important due to effect on
[photosynthate] in guard cells
PHOT1 &2 also help
Main GC blue
receptor is zeaxanthin!
Reason for green reversal
water stress overrides light!

73. Phototropins
water stress overrides light: roots make Abscisic Acid: closes stomates & blocks opening regardless of other signals!