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

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

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)

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!

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)

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

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

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

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 higher @ 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

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 higher @ 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

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 higher @ 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

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

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

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

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

Blue Light Responses Circadian Rhythms

Blue Light Responses Circadian Rhythms Solar tracking

Blue Light Responses Circadian Rhythms Solar tracking Phototropism

Blue Light Responses Circadian Rhythms Solar tracking Phototropism Inhibiting stem elongation

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

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

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

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

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

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

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

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!

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

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

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

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

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!)

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

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

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)

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

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

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

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

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

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

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

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

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

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

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

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!

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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+

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+

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

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

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

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

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

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

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!

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

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!

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