How bacteria regulate cell cycle progression at a molecular level is a fundamental but poorly understood problem. In Caulobacter crescentus, two-component signal transduction proteins are crucial for cell cycle regulation, but the connectivity of regulators involved has remained elusive and key factors are unidentified. Here we identify ChpT, an essential histidine phosphotransferase that controls the activity of CtrA, the master cell cycle regulator. We show that the essential histidine kinase CckA initiates two phosphorelays, each requiring ChpT, which lead to the phosphorylation and stabilization of CtrA. Downregulation of CckA activity therefore results in the dephosphorylation and degradation of CtrA, which in turn allow the initiation of DNA replication. Furthermore, we show that CtrA triggers its own destruction by promoting cell division and inducing synthesis of the essential regulator DivK, which feeds back to downregulate CckA immediately before S phase. Our results define a single integrated circuit whose components and connectivity can account for the cell cycle oscillations of CtrA in Caulobacter.
Leaf senescence is a key physiological process in all plants. Its onset is tightly controlled by transcription factors, of which NAC factor ORE1 (ANAC092) is crucial in Arabidopsis thaliana. Enhanced expression of ORE1 triggers early senescence by controlling a downstream gene network that includes various senescence-associated genes. Here, we report that unexpectedly ORE1 interacts with the G2-like transcription factors GLK1 and GLK2, which are important for chloroplast development and maintenance, and thereby for leaf maintenance. ORE1 antagonizes GLK transcriptional activity, shifting the balance from chloroplast maintenance towards deterioration. Our finding identifies a new mechanism important for the control of senescence by ORE1.Keywords: transcription factor; senescence; chloroplast; protein-protein interaction EMBO reports (2013EMBO reports ( ) 14, 382-388. doi:10.1038EMBO reports ( /embor.2013 INTRODUCTIONLeaf senescence is a developmentally controlled process that involves extensive reprogramming and modulation of gene expression to maximize plant fitness by remobilizing nutrients from deteriorating leaves to newly growing vegetative and reproductive organs. Early and noticeable features of leaf senescence are Rubisco and chlorophyll degradation, and a decline of photosynthetic activity owing to chloroplast dismantling [1,2]. Transcription factors (TFs) have important roles in coordinating the gene regulatory networks that underlie the senescence process [3,4]. One of the key senescence-control TF in A. thaliana is the NAC protein ORE1 (ANAC092; At5g39610). Overexpression of ORE1 in transgenic plants triggers early senescence, while its inhibition retards senescence [5,6]. ORE1 exerts its regulatory function by controlling the expression of various known senescence-associated genes (SAGs) [5]. Expression of ORE1 itself is controlled by at least two molecular mechanisms, one that involves currently unknown upstream TFs that determine leaf age-and abiotic stress-dependent ORE1 transcriptional activity [5], and a second one that leads to ORE1 messenger RNA degradation by transacting miR164 [6]. Both processes contribute to establishing a coordinated expression of ORE1, which is low in young, but high in aging leaves.In an aging leaf, the onset of senescence is counterbalanced by still vaguely defined chloroplast maintenance mechanisms. Key elements in this process are the Golden2-like TFs that act as nuclear regulators of chloroplast development and maintenance by coordinating the expression of genes-encoding proteins of the photosynthetic apparatus in various plant species, including A. thaliana, Zea mays and the moss Physcomitrella patens [7,8]. In Arabidopsis, GLK genes exist as a pair of homologous genes, GLK1 and GLK2, and they have been shown to be functionally redundant such that only glk1/glk2 double mutants show a clear phenotype [7,8].Herein, we report the unexpected finding that ORE1 interacts with GLK TFs at the protein level. Elevated expression of ORE1 in the presence of GLK expression str...
SummaryA fundamental question in developmental biology is how morphogenesis is coordinated with cell cycle progression. In Caulobacter crescentus , each cell cycle produces morphologically distinct daughter cells, a stalked cell and a flagellated swarmer cell. Construction of both the flagellum and stalk requires the alternative sigma factor RpoN ( σ σ σ σ 54). Here we report that a σ σ σ σ 54-dependent activator, TacA, is required for cell cycle regulated stalk biogenesis by collaborating with RpoN to activate gene expression. We have also identified the first histidine phosphotransferase in C. crescentus , ShpA, and show that it too is required for stalk biogenesis. Using a systematic biochemical technique called phosphotransfer profiling we have identified a multicomponent phosphorelay which leads from the hybrid histidine kinase ShkA to ShpA and finally to TacA. This pathway functions in vivo to phosphorylate and hence, activate TacA. Finally, whole genome microarrays were used to identify candidate members of the TacA regulon, and we show that at least one target gene, staR , regulates stalk length. This is the first example of a general method for identifying the connectivity of a phosphorelay and can be applied to any organism with two-component signal transduction systems.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.