Sigma factor (
Plant development requires communication on many levels, including between cells and between organelles within a cell. For example, mitochondria and plastids have been proposed to be sensors of environmental stress and to coordinate their responses. Here we present evidence for communication between mitochondria and chloroplasts during leaf and root development, based on genetic and physical interactions between three
- NSF-PAR ID:
- 10089343
- Publisher / Repository:
- Wiley Blackwell (John Wiley & Sons)
- Date Published:
- Journal Name:
- Plant Direct
- Volume:
- 3
- Issue:
- 3
- ISSN:
- 2475-4455
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Abstract SIG ) proteins contribute to promoter specificity of the plastid‐encodedRNA polymerase during chloroplast genome transcription. All six members of theSIG family, that is,SIG 1–SIG 6, are nuclear‐encoded proteins targeted to chloroplasts. Sigma factor 2 (SIG 2) is a phytochrome‐regulated protein important for stoichiometric control of the expression of plastid‐ and nuclear‐encoded genes that impact plastid development and plant growth and development. AmongSIG factors,SIG 2 is required not only for transcription of chloroplast genes (i.e., anterograde signaling), but also impacts nuclear‐encoded, photosynthesis‐related, and light signaling‐related genes (i.e., retrograde signaling) in response to plastid functional status. AlthoughSIG 2 is involved in photomorphogenesis in Arabidopsis, the molecular bases for its role in light signaling that impacts photomorphogenesis and aspects of photosynthesis have only recently begun to be investigated. Previously, we reported thatSIG 2 is necessary for phytochrome‐mediated photomorphogenesis specifically under red (R) and far‐red light, thereby suggesting a link between phytochromes and nuclear‐encodedSIG 2 in light signaling. To explore transcriptional roles ofSIG 2 in R‐dependent growth and development, we performedRNA sequencing analysis to compare gene expression insig2‐2 mutant and Col‐0 wild‐type seedlings at two developmental stages (1‐ and 7‐day). We identified a subset of misregulated genes involved in growth, hormonal cross talk, stress responses, and photosynthesis. To investigate the functional relevance of these gene expression analyses, we performed several comparative phenotyping tests. In these analyses, strongsig2 mutants showed insensitivity to bioactiveGA 3, high intracellular levels of hydrogen peroxide (H2O2) indicative of a stress response, and specific defects in photosynthesis, including elevated levels of cyclic electron flow (CEF ) and nonphotochemical quenching (NPQ ). We demonstrated thatSIG 2 regulates a broader range of physiological responses at the molecular level than previously reported, with specific roles in red‐light‐mediated photomorphogenesis. -
Premise Light is critical in the ability of plants to accumulate chlorophyll. When exposed to far‐red (
FR ) light and then grown in white light in the absence of sucrose, wild‐type seedlings fail to green in a response known as theFR block of greening (BOG ). This response is controlled by phytochrome A through repression of protochlorophyllide reductase‐encoding (POR ) genes byFR light coupled with irreversible plastid damage. Sigma (SIG ) factors are nuclear‐encoded proteins that contribute to plant greening and plastid development through regulating gene transcription in chloroplasts and impacting retrograde signaling from the plastid to nucleus.SIG s are regulated by phytochromes, and the expression of someSIG factors is reduced in phytochrome mutant lines, includingphyA . Given the association of phyA with theFR BOG and its regulation ofSIG factors, we investigated the potential regulatory role ofSIG factors in theFR BOG response.Methods We examined
FR BOG responses insig mutants, phytochrome‐deficient lines, and mutant lines for several phy‐associated factors. We quantified chlorophyll levels and examined expression of keyBOG ‐associated genes.Results Among six
sig mutants, only thesig6 mutant significantly accumulated chlorophyll afterFR BOG treatment, similar to thephyA mutant.SIG 6 appears to control protochlorophyllide accumulation by contributing to the regulation of tetrapyrrole biosynthesis associated with glutamyl‐tRNA reductase (HEMA 1) function, select phytochrome‐interacting factor genes (PIF4 andPIF6 ), andPENTA1 , which regulatesPORA mRNA translation afterFR exposure.Conclusions Regulation of
SIG6 plays a significant role in plant responses toFR exposure during theBOG response. -
Summary Malonyl‐CoA is a key intermediate in a number of metabolic processes associated with its role as a substrate in acylation and condensation reactions. These types of reactions occur in plastids, the cytosol and mitochondria, and although carboxylation of acetyl‐CoA is the known mechanism for generating the distinct plastidial and cytosolic pools, the metabolic origin of the mitochondrial malonyl‐CoA pool is still unclear. In this study we demonstrate that malonyl‐CoA synthetase encoded by the Arabidopsis
(AAE 13 ) gene is localized in both the cytosol and the mitochondria. These isoforms are translated from two types of transcripts, one that contains and one that does not contain a mitochondrial‐targeting pre‐sequence. Whereas the cytosolicAT 3G16170AAE 13 protein is not essential, due to the presence of a redundant malonyl‐CoA generating system provided by a cytosolic acetyl‐CoA carboxylase, the mitochondrialAAE 13 protein is essential for plant growth. Phenotypes of theaae13‐1 mutant are transgenically reversed only if the mitochondrial pre‐sequence is present in the ectopically expressedAAE 13 proteins. Theaae13‐1 mutant exhibits typical metabolic phenotypes associated with a deficiency in the mitochondrial fatty acid synthase system, namely depleted lipoylation of the H subunit of the photorespiratory enzyme glycine decarboxylase, increased accumulation of glycine and glycolate and reduced levels of sucrose. Most of these metabolic alterations, and associated morphological changes, are reversed when theaae13‐1 mutant is grown in a non‐photorespiratory condition (i.e. a 1%CO 2atmosphere), demonstrating that they are a consequence of the deficiency in photorespiration due to the inability to generate lipoic acid from mitochondrially synthesized fatty acids. -
Summary Cytosolic calcium concentration ([Ca2+]cyt) and heterotrimeric G‐proteins are universal eukaryotic signaling elements. In plant guard cells, extracellular calcium (Cao) is as strong a stimulus for stomatal closure as the phytohormone abscisic acid (
ABA ), but underlying mechanisms remain elusive. Here, we report that the sole Arabidopsis heterotrimeric Gβ subunit,AGB 1, is required for four guard cell Caoresponses: induction of stomatal closure; inhibition of stomatal opening; [Ca2+]cytoscillation; and inositol 1,4,5‐trisphosphate (InsP3) production. Stomata in wild‐type Arabidopsis (Col) and in mutants of the canonical Gα subunit, , showed inhibition of stomatal opening and promotion of stomatal closure by Cao. By contrast, stomatal movements ofGPA 1agb1 mutants andagb1 /gpa1 double‐mutants, as well as those of theagg1agg2 Gγ double‐mutant, were insensitive to Cao. These behaviors contrast withABA ‐regulated stomatal movements, which involveGPA 1 andAGB 1/AGG 3 dimers, illustrating differential partitioning of G‐protein subunits among stimuli with similar ultimate impacts, which may facilitate stimulus‐specific encoding. knockouts retained reactive oxygen species andAGB 1NO production, but lostYC 3.6‐detected [Ca2+]cytoscillations in response to Cao, initiating only a single [Ca2+]cytspike. Experimentally imposed [Ca2+]cytoscillations restored stomatal closure inagb1 . Yeast two‐hybrid and bimolecular complementation fluorescence experiments revealed thatAGB 1 interacts with phospholipase Cs (PLCs), and Caoinduced InsP3 production in Col but not inagb1 . In sum, G‐protein signaling viaAGB 1/AGG 1/AGG 2 is essential for Cao‐regulation of stomatal apertures, and stomatal movements in response to Caoapparently require Ca2+‐induced Ca2+release that is likely dependent on Gβγ interaction withPLC s leading to InsP3 production. -
Summary Catabolism of fatty acids stored in oil bodies is essential for seed germination and seedling development in Arabidopsis. This fatty acid breakdown occurs in peroxisomes, organelles that sequester oxidative reactions. Import of peroxisomal enzymes is facilitated by peroxins including
PEX 5, a receptor that delivers cargo proteins from the cytosol to the peroxisomal matrix. After cargo delivery, a complex of thePEX 1 andPEX 6ATP ases and thePEX 26 tail‐anchored membrane protein removes ubiquitinatedPEX 5 from the peroxisomal membrane. We identified Arabidopsispex6 andpex26 mutants by screening for inefficient seedling β‐oxidation phenotypes. The mutants displayed distinct defects in growth, response to a peroxisomally metabolized auxin precursor, and peroxisomal protein import. The lowPEX 5 levels in these mutants were increased by treatment with a proteasome inhibitor or by combiningpex26 with peroxisome‐associated ubiquitination machinery mutants, suggesting that ubiquitinatedPEX 5 is degraded by the proteasome when the function ofPEX 6 orPEX 26 is reduced. Combiningpex26 with mutations that increasePEX 5 levels either worsened or improvedpex26 physiological and molecular defects, depending on the introduced lesion. Moreover, elevatingPEX 5 levels via a35S: transgene exacerbatedPEX 5pex26 defects and ameliorated the defects of only a subset ofpex6 alleles, implying that decreasedPEX 5 is not the sole molecular deficiency in these mutants. We found peroxisomes clustered around persisting oil bodies inpex6 andpex26 seedlings, suggesting a role for peroxisomal retrotranslocation machinery in oil body utilization. The disparate phenotypes of thesepex alleles may reflect unanticipated functions of the peroxisomalATP ase complex.