Plastid-nucleus communication involves calcium-modulated MAPK signalling

Chloroplast retrograde signals play important roles in coordinating the plastid and nuclear gene expression and are critical for proper chloroplast biogenesis and for maintaining optimal chloroplast functions in response to environmental changes in plants. Until now, the signals and the mechanisms for retrograde signalling remain poorly understood. Here we identify factors that allow the nucleus to perceive stress conditions in the chloroplast and to respond accordingly by inducing or repressing specific nuclear genes encoding plastid proteins. We show that ABI4, which is known to repress the LHCB genes during retrograde signalling, is activated through phosphorylation by the MAP kinases MPK3/MPK6 and the activity of these kinases is regulated through 14-3-3 omega-mediated Ca2+-dependent scaffolding depending on the chloroplast calcium sensor protein CAS. These findings uncover an additional mechanism in which chloroplast-modulated Ca2+ signalling controls the MAPK pathway for the activation of critical components of the retrograde signalling chain

Plastid-nucleus communication involves calcium-modulated MAPK signalling

Chloroplast retrograde signals play important roles in coordinating the plastid and nuclear gene expression and are critical for proper chloroplast biogenesis and for maintaining optimal chloroplast functions in response to environmental changes in plants. Until now, the signals and the mechanisms for retrograde signalling remain poorly understood. Here we identify factors that allow the nucleus to perceive stress conditions in the chloroplast and to respond accordingly by inducing or repressing specific nuclear genes encoding plastid proteins. We show that ABI4, which is known to repress the LHCB genes during retrograde signalling, is activated through phosphorylation by the MAP kinases MPK3/MPK6 and the activity of these kinases is regulated through 14-3-3 omega-mediated Ca2+-dependent scaffolding depending on the chloroplast calcium sensor protein CAS. These findings uncover an additional mechanism in which chloroplast-modulated Ca2+ signalling controls the MAPK pathway for the activation of critical components of the retrograde signalling chain

Convergence of light and chloroplast signals for de-etiolation through ABI4-HY5 and COP1.

Seedling de-etiolation prepares plants to switch from heterotrophic to photoautotrophic growth, a transition essential for plant survival. This delicate de-etiolation process is precisely controlled by environmental and endogenous signals. Although intracellular plastid-derived retrograde signalling is essential for the de-etiolation process, the molecular nature of these retrograde signals remains elusive(1-3). Here we show that chloroplast and light signals antagonistically fine-tune a suite of developmental and physiological responses associated with de-etiolation through a transcriptional module of ABA INSENSITIVE 4 (ABI4) and ELONGATED HYPOCOTYL 5 (HY5). Moreover, ABI4 and HY5 antagonistically regulate the expression of CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1) and the subsequent greening process. In turn, ABI4 and HY5 are targeted for degradation by COP1 in the light and dark, respectively, to ensure a proper interplay of ABI4 and HY5 actions during seedling de-etiolation. Our study provides a new molecular mechanism for understanding how chloroplast signals converge with light signals to optimize early plant development

Convergence of light and chloroplast signals for de-etiolation through ABI4-HY5 and COP1

Seedling de-etiolation prepares plants to switch from heterotrophic to photoautotrophic growth, a transition essential for plant survival. This delicate de-etiolation process is precisely controlled by environmental and endogenous signals. Although intracellular plastid-derived retrograde signalling is essential for the de-etiolation process, the molecular nature of these retrograde signals remains elusive(1-3). Here we show that chloroplast and light signals antagonistically fine-tune a suite of developmental and physiological responses associated with de-etiolation through a transcriptional module of ABA INSENSITIVE 4 (ABI4) and ELONGATED HYPOCOTYL 5 (HY5). Moreover, ABI4 and HY5 antagonistically regulate the expression of CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1) and the subsequent greening process. In turn, ABI4 and HY5 are targeted for degradation by COP1 in the light and dark, respectively, to ensure a proper interplay of ABI4 and HY5 actions during seedling de-etiolation. Our study provides a new molecular mechanism for understanding how chloroplast signals converge with light signals to optimize early plant development

Plastid-nucleus communication involves calcium-modulated MAPK signalling

Chloroplast retrograde signals play important roles in coordinating the plastid and nuclear gene expression and are critical for proper chloroplast biogenesis and for maintaining optimal chloroplast functions in response to environmental changes in plants. Until now, the signals and the mechanisms for retrograde signalling remain poorly understood. Here we identify factors that allow the nucleus to perceive stress conditions in the chloroplast and to respond accordingly by inducing or repressing specific nuclear genes encoding plastid proteins. We show that ABI4, which is known to repress the LHCB genes during retrograde signalling, is activated through phosphorylation by the MAP kinases MPK3/MPK6 and the activity of these kinases is regulated through 14-3-3 omega-mediated Ca2+-dependent scaffolding depending on the chloroplast calcium sensor protein CAS. These findings uncover an additional mechanism in which chloroplast-modulated Ca2+ signalling controls the MAPK pathway for the activation of critical components of the retrograde signalling chain

Chloroplast retrograde signal regulates flowering

Light is a major environmental factor regulating flowering time, thus ensuring reproductive success of higher plants. In contrast to our detailed understanding of light quality and photoperiod mechanisms involved, the molecular basis underlying high light-promoted flowering remains elusive. Here we show that, in Arabidopsis, a chloroplast-derived signal is critical for high light-regulated flowering mediated by the FLOWERING LOCUS C (FLC). We also demonstrate that PTM, a PHD transcription factor involved in chloroplast retrograde signaling, perceives such a signal and mediates transcriptional repression of FLC through recruitment of FVE, a component of the histone deacetylase complex. Thus, our data suggest that chloroplasts function as essential sensors of high light to regulate flowering and adaptive responses by triggering nuclear transcriptional changes at the chromatin level

Chloroplast retrograde signal regulates flowering

Light is a major environmental factor regulating flowering time, thus ensuring reproductive success of higher plants. In contrast to our detailed understanding of light quality and photoperiod mechanisms involved, the molecular basis underlying high light-promoted flowering remains elusive. Here we show that, in Arabidopsis, a chloroplast-derived signal is critical for high light-regulated flowering mediated by the FLOWERING LOCUS C (FLC). We also demonstrate that PTM, a PHD transcription factor involved in chloroplast retrograde signaling, perceives such a signal and mediates transcriptional repression of FLC through recruitment of FVE, a component of the histone deacetylase complex. Thus, our data suggest that chloroplasts function as essential sensors of high light to regulate flowering and adaptive responses by triggering nuclear transcriptional changes at the chromatin level