Plant Physiology最新文献

Autophagy is a vesicular mechanism that plays a fundamental role in nitrogen remobilization from senescing leaves to seeds. The Arabidopsis (Arabidopsis thaliana) autophagy (atg) mutants exhibit early senescence, reduced biomass, and low seed yield. The atg seeds also exhibit major changes in N and C concentrations. During plant development, autophagy genes are expressed in the source leaves and in the sink seeds during maturation. We thus addressed the question of whether the seed composition defects in atg mutants are caused by defective N remobilization from source leaves or whether they are due to the absence of autophagy in seeds during maturation. To answer this question, we restored autophagy activity in the atg5 mutant by expressing the wild-type (WT) ATG5 allele specifically in source leaves using the senescence-associated gene 12 (SAG12) promoter or specifically in seeds using the Glycinin-1 promoter, or in both organs using both constructs. In atg5, N remobilization from the rosettes to seeds was almost completely reestablished when transformed with the pSAG12::ATG5 construct. However, transformation with the pSAG12::ATG5 construct only partially restored seed composition. In contrast, seed N and C composition was largely restored by transformation with the pGly::ATG5 construct, even though the early leaf senescence phenotype was maintained in the atg5 background. Cotransformation with pSAG12::ATG5 and pGly::ATG5 completely restored the WT remobilization and seed composition phenotypes. Our results highlight the essential role of autophagy in leaves for nitrogen supply and in seeds for the establishment of carbon and nitrogen reserves.

Sphingolipid homeostatic regulation is important for balancing plant life and death. Plant cells finely tune sphingolipid biosynthesis to ensure sufficient levels to support growth through their basal functions as major components of endomembranes and the plasma membrane. Conversely, accumulation of sphingolipid biosynthetic intermediates, long-chain bases (LCBs) and ceramides, is associated with programmed cell death. Limiting these apoptotic intermediates is important for cell viability, while overriding homeostatic regulation permits cells to generate elevated LCBs and ceramides to respond to pathogens to elicit the hypersensitive response in plant immunity. Key to sphingolipid homeostasis is serine palmitoyltransferase (SPT), an endoplasmic reticulum-associated, multi-subunit enzyme catalyzing the first step in the biosynthesis of LCBs, the defining feature of sphingolipids. Across eukaryotes, SPT interaction with its negative regulator Orosomucoid-like (ORM) is critical for sphingolipid biosynthetic homeostasis. The recent cryo-electron microscopy structure of the Arabidopsis SPT complex indicates that ceramides bind ORMs to competitively inhibit SPT activity. This system provides a sensor for intracellular ceramide concentrations for sphingolipid homeostatic regulation. Combining the newly elucidated Arabidopsis SPT structure and mutant characterization, we present a model for the role of the 2 functionally divergent Arabidopsis ceramide synthase classes to produce ceramides that form repressive (trihydroxy LCB-ceramides) or nonrepressive (dihydroxy LCB-ceramides) ORM interactions to influence SPT activity. We describe how sphingolipid biosynthesis is regulated by the interplay of ceramide synthases with ORM-SPT when "enough is enough" and override homeostatic suppression when "enough is not enough" to respond to environmental stimuli such as microbial pathogen attack.

Nitrogen (N) scarcity frequently constrains global biomass productivity. N deficiency halts cell division, downregulates photosynthetic electron transfer (PET), and enhances carbon storage. However, the molecular mechanism downregulating photosynthesis during N deficiency and its relationship with carbon storage are not fully understood. Proton gradient regulator-like 1 (PGRL1) controlling cyclic electron flow (CEF) and flavodiiron proteins (FLV) involved in pseudo-CEF (PCEF) are major players in the acclimation of photosynthesis. To determine the role of PGRL1 or FLV in photosynthesis under N deficiency, we measured PET, oxygen gas exchange, and carbon storage in Chlamydomonas reinhardtii pgrl1 and flvB knockout mutants. Under N deficiency, pgrl1 maintained higher net photosynthesis and O2 photoreduction rates and higher levels of cytochrome b6f and PSI compared with the control and flvB. The photosynthetic activity of flvB and pgrl1 flvB double mutants decreased in response to N deficiency, similar to the control strains. Furthermore, the preservation of photosynthetic activity in pgrl1 was accompanied by an increased accumulation of triacylglycerol in certain genetic backgrounds but not all, highlighting the importance of gene-environment interaction in determining traits such as oil content. Our results suggest that in the absence of PGRL1-controlled CEF, FLV-mediated PCEF maintains net photosynthesis at a high level and that CEF and PCEF play antagonistic roles during N deficiency. This study further illustrate how a strain's nutrient status and genetic makeup can affect the regulation of photosynthetic energy conversion in relation to carbon storage and provide additional strategies for improving lipid productivity in algae.

As major contributors to flavor in many fruit species, volatile esters are useful for investigating the regulation of the biosynthesis pathways of volatile aroma compounds in plants. Ethylene promotes the biosynthesis of volatile esters during fruit storage while accelerating fruit ripening; thus, the ethylene perception inhibitor 1-methylcyclopropene (1-MCP) is employed to prolong the shelf life of fruits. However, the mechanisms by which 1-MCP regulates volatiles synthesis remain unclear. In this study, we analyzed the pathway of 1-MCP-mediated volatile ester synthesis in 'Nanguo' pear (Pyrus ussuriensis). 1-MCP significantly decreased volatile ester synthesis during storage. Comparative transcriptome analysis showed that the genes encoding two transcription factors (PuNAC37 and PuWRKY74) and a RING-type E3 ubiquitin ligase that have a domain of unknown function (PuRDUF2) were expressed at high levels, whereas ALCOHOL ACYLTRANSFERASE 1 (PuAAT1), encoding an enzyme responsible for volatile ester synthesis, was expressed at low levels in 1-MCP-treated fruit. Moreover, PuNAC37 inhibited the expression of PuWRKY74 via transcriptional regulation, whereas PuNAC37 and PuWRKY74, after directly binding to the promoter of PuAAT1, synergistically inhibited its expression in 1-MCP-treated fruit. In addition, in vitro and in vivo ubiquitination experiments revealed that PuRDUF2 functions as an E3 ubiquitin ligase that ubiquitinates PuAAT1, causing its degradation via the 26S proteasome pathway following 1-MCP treatment. Subsequent PuAAT1 degradation resulted in a reduction of volatile esters during fruit storage. Our findings provide insights into the complex transcriptional regulation of volatile ester formation in 'Nanguo' pears and contribute to future research on AAT protein ubiquitination in other species.

CALCIUM-DEPENDENT PROTEIN KINASE (CDPK) stimulates reactive oxygen species (ROS)-dependent signaling by activating RESPIRATORY BURST OXIDASE HOMOLOG (RBOH). The lysigenous aerenchyma is a gas space created by cortical cell death that facilitates oxygen diffusion from the shoot to the root tips. Previously, we showed that RBOHH is indispensable for the induction of aerenchyma formation in rice (Oryza sativa) roots under low-oxygen conditions. Here, we showed that CDPK5 and CDPK13 localize to the plasma membrane where RBOHH functions. Mutation analysis of the serine at residues 92 and 107 of RBOHH revealed that these residues are required for CDPK5- and CDPK13-mediated activation of ROS production. The requirement of Ca2+ for CDPK5 and CDPK13 function was confirmed using in vitro kinase assays. CRISPR/Cas9-based mutagenesis of CDPK5 and/or CDPK13 revealed that the double knockout almost completely suppressed inducible aerenchyma formation, whereas the effects were limited in the single knockout of either CDPK5 or CDPK13. Interestingly, the double knockout almost suppressed the induction of adventitious root formation, which is widely conserved in vascular plants, under low-oxygen conditions. Our results suggest that CDPKs are essential for the acclimation of rice to low-oxygen conditions and also for many other plant species conserving CDPK-targeted phosphorylation sites in RBOH homologs.

Enhanced autoimmunity often leads to impaired plant growth and development, and the coordination of immunity and growth in Populus remains elusive. In this study, we have identified the transcription factors PagWRKY33a/b as key regulators of immune response and growth maintenance in Populus. The disruption of PagWRKY33a/b causes growth issues and autoimmunity while conferring resistance to anthracnose caused by Colletotrichum gloeosporioides. PagWRKY33a/b binds to the promoters of N requirement gene 1.1 (NRG1.1) and Gibberellic Acid-Stimulated in Arabidopsis (GASA14) during infection, activating their transcription. This process maintains disease resistance and engages in GA signaling to reduce growth costs from immune activation. The oxPagWRKY33a/nrg1.1 mutant results in reduced resistance to C. gloeosporioides. Further, PagWRKY33a/b is phosphorylated and activated by mitogen-activated protein kinase kinase 1, which inhibits respiratory burst oxidase homolog D (RBOHD) and respiratory burst oxidase homolog I (RBOHI) transcription, causing reactive oxygen species bursts in wrky33a/b double mutants. This leads to an upregulation of PagNRG1.1 in the absence of pathogens. However, the wrky33a/b/nrg1.1 and wrky33a/b/rbohd triple mutants show compromised defense responses, underscoring the complexity of WRKY33 regulation. Additionally, the stability of PagWRKY33 is modulated by Ring Finger Protein 5 (PagRNF5)-mediated ubiquitination, balancing plant immunity and growth. Together, our results provide key insights into the complex function of WRKY33 in Populus autoimmunity and its impact on growth and development.