Among the major phytohormones, the cytokinin exhibits unique features for its ability to positively affect the developmental status of plastids. Even early on in its research, cytokinins were known to promote plastid differentiation and to reduce the loss of chlorophyll in detached leaves. Since the discovery of the components of cytokinin perception and primary signaling, the genes involved in photosynthesis and plastid differentiation have been identified as those directly targeted by type-B response regulators. Furthermore, cytokinins are known to modulate versatile cellular processes such as promoting the division and differentiation of cells and, in concert with auxin, initiating the de novo formation of shoot apical meristem (SAM) in tissue cultures. Yet how cytokinins precisely participate in such diverse cellular phenomena, and how the associated cellular processes are coordinated as a whole, remains unclear. A plausible presumption that would account for the coordinated gene expression is the tight and reciprocal communication between the nucleus and plastid. The fact that cytokinins affect plastid developmental status via gene expression in both the nucleus and plastid is interpreted here to suggest that cytokinin functions as an initiator of anterograde (nucleus-to-plastid) signaling. Based on this viewpoint, we first summarize the physiological relevance of cytokinins to the coordination of plastid differentiation with de novo shoot organogenesis in tissue culture systems. Next, the role of endogenous cytokinins in influencing plastid differentiation within the SAM of intact plants is discussed. Finally, a presumed plastid-derived signal in response to cytokinins for coupled nuclear gene expression is proposed.

Biogenesis of chloroplasts in higher plants is initiated from proplastids, and involves a series of processes by which a plastid able to perform photosynthesis, to synthesize amino acids, lipids, and phytohormones is formed. All plastid protein complexes are composed of subunits encoded by the nucleus and chloroplast genomes, which require a coordinated gene expression to produce the correct concentrations of organellar proteins and to maintain organelle function. To achieve this, hundreds of nucleus-encoded factors are imported into the chloroplast to control plastid gene expression. Among these factors, members of the Pentatricopeptide Repeat (PPR) containing protein family have emerged as key regulators of the organellar post-transcriptional processing. PPR proteins represent a large family in plants, and the extent to which PPR functions are conserved between dicots and monocots deserves evaluation, in light of differences in photosynthetic metabolism (C3 vs. C4) and localization of chloroplast biogenesis (mesophyll vs. bundle sheath cells). In this work we investigated the role played in the process of chloroplast biogenesis by At5g42310, a member of the Arabidopsis PPR family which we here refer to as AtCRP1 (Chloroplast RNA Processing 1), providing a comparison with the orthologous ZmCRP1 protein from Zea mays. Loss-of-function atcrp1 mutants are characterized by yellow-albinotic cotyledons and leaves owing to defects in the accumulation of subunits of the thylakoid protein complexes. As in the case of ZmCRP1, AtCRP1 associates with the 5\' UTRs of both psaC and, albeit very weakly, petA transcripts, indicating that the role of CRP1 as regulator of chloroplast protein synthesis has been conserved between maize and Arabidopsis. AtCRP1 also interacts with the petB-petD intergenic region and is required for the generation of petB and petD monocistronic RNAs. A similar role has been also attributed to ZmCRP1, although the direct interaction of ZmCRP1 with the petB-petD intergenic region has never been reported, which could indicate that AtCRP1 and ZmCRP1 differ, in part, in their plastid RNA targets.

The coordination of nuclear and mitochondrial genomes plays a pivotal role in maintenance of mitochondrial biogenesis and functionality during stress and aging. Environmental and cellular inputs signal to nucleus and/or mitochondria to trigger interorganellar compensatory responses. Loss of this tightly orchestrated coordination results in loss of cellular homeostasis and underlies various pathologies and age-related diseases. Several signaling cascades that govern interorganellar communication have been revealed up to now, and have been classified as part of the anterograde (nucleus to mitochondria) or retrograde (mitochondrial to nucleus) response. Many of these molecular pathways rely on the dual distribution of nuclear or mitochondrial components under basal or stress conditions. These dually localized components usually engage in specific tasks in their primary organelle of function, whilst upon cellular stimuli, they appear in the other organelle where they engage in the same or a different task, triggering a compensatory stress response. In this review, we focus on protein factors distributed between the nucleus and mitochondria and activated to exert their functions upon basal or stress conditions. We further discuss implications of bi-organellar targeting in the context of aging.

Retrograde signaling, defined as the signaling events leading from the plastids to the nucleus, coordinates the expression of plastid and nuclear genes and is crucial for metabolic as well as developmental processes of the plastids. In the recent past, the identification of various components that are involved in the generation and transmission of plastid-originated retrograde signals and the regulation of nuclear gene expression has only provided a glimpse of the plastid retrograde signaling network, which remains poorly understood. The basic assumptions underlying our current understanding of retrograde signaling stayed untouched for many years. Therefore, an attempt has been made in this review article to summarize established facts and recent advances regarding various retrograde signaling pathways derived from different sources, the identification of key elements mediating retrograde signal transduction and also to give an overview of possible signaling molecules that remain to be investigated.

Light perception by photoreceptors impacts plastid transcription, development, and differentiation. This photoreceptor-dependent activity suggests a mechanism for photoregulation of gene expression in the nucleus and plastid that serves to coordinate expression of critical genes of these two organelles. This coordinate expression is required for proper stoichiometric accumulation of components needed for assembly of plastids, photosynthetic light-harvesting complexes and components such as phytochromes. Chloroplast-targeted sigma factors, which function together with the plastid-encoded RNA polymerase to regulate expression of plastid-encoded genes, and nuclear-encoded plastid development factors, such as GLK1 and GLK2, are targets of phytochrome regulation. Such phytochrome-dependent functions are hypothesized to allow light-dependent regulation, and feasibly tuning, of plastid components and function in response to changes in the external environment, which directly affects photosynthesis and the potential for light-induced damage. When the size and protein composition of the light-harvesting complexes are not tuned to the external environment, imbalances in electron transport can impact the cellular redox state and cause cellular damage. We show that phytochromes specifically regulate the expression of multiple factors that function to modulate plastid transcription and, thus, provide a paradigm for coordinate expression of the nuclear and plastid genomes in response to changes in external light conditions. As phytochromes respond to changes in the prevalent wavelengths of light and light intensity, we propose that specific phytochrome-dependent molecular mechanisms are used during light-dependent signaling between the nucleus and chloroplast during photomorphogenesis to coordinate chloroplast development with plant developmental stage and the external environment.