Plant Cell最新文献

Maize (Zea mays L.) is a global crop species in which CO2 assimilation occurs via the C4 pathway. C4 photosynthesis is typically more efficient than C3 photosynthesis under warm and dry conditions; however, despite this inherent advantage, considerable variation remains in photosynthetic efficiency for C4 species that could be leveraged to benefit crop performance. Here, we investigate the genetic architecture of nonphotochemical quenching (NPQ) and photosystem II (PSII) efficiency using a combination of high-throughput phenotyping and quantitative trait loci (QTL) mapping in a field-grown Multi-parent Advanced Generation Inter-Cross (MAGIC) mapping population. QTL mapping was followed by the identification of putative candidate genes using a combination of genomics, transcriptomics, protein biochemistry, and targeted physiological phenotyping. We identified four genes with a putative causal role in the observed QTL effects. The highest confidence causal gene was found for a large effect QTL for photosynthetic efficiency on chromosome 10, which was underpinned by allelic variation in the expression of the minor PSII antenna protein light harvesting complex photosystem II subunit (LHCB6 or CP24), mainly driven by poor expression associated with the haplotype of the F7 founder line. The historical role of this line in breeding for early flowering time may suggest that the presence of this deficient allele could be enriched in temperate maize germplasm. These findings advance our understanding of the genetic basis of NPQ and PSII efficiency in C4 plants and highlight the potential for breeding strategies aimed at optimizing photosynthetic efficiency in maize.

Chlorophyll biosynthesis must be tightly coupled to light-harvesting chlorophyll a/b-binding protein (LHCP) biogenesis, as free chlorophyll and its precursors are phototoxic. However, precisely how these 2 processes are coordinated in Arabidopsis (Arabidopsis thaliana) remains elusive. Our previous studies demonstrated the role of LHCP TRANSLOCATION DEFECT (LTD) in delivering LHCPs to the chloroplast via the signal recognition particle-dependent pathway. Here, we show that LTD interacts with and stabilizes the chlorophyll biosynthesis enzymes Mg-protoporphyrin methyltransferase and Mg-protoporphyrin monomethylester (MgPME) cyclase, maintaining their activity. We also demonstrate the direct binding of LTD to MgPME, and through crystal structure analysis, we show that the groove of the LTD dimer is critical for MgPME binding. Thus, we propose that LTD transfers MgPME from Mg-protoporphyrin methyltransferase to the MgPME cyclase. These results elucidate a role for LTD in synchronizing chlorophyll biosynthesis with LHCP transport to ensure the correct insertion of chlorophylls into LHCPs.

In Arabidopsis (Arabidopsis thaliana), MICRORCHIDIA 1 (MORC1), a member of the MORC family of evolutionarily conserved GHKL-type ATPases, plays important roles in multiple layers of plant immunity. However, the molecular mechanism by which MORC1 regulates plant immunity remains obscure. Here, we report that the pathogen-responsive kinase CALCIUM-DEPENDENT PROTEIN KINASE 5 (CPK5) directly interacts with and phosphorylates MORC1, thereby promoting its stability and nuclear translocation. In the nucleus, MORC1 associates with the NONEXPRESSOR OF PATHOGENESIS-RELATED GENES 1 (NPR1)-TGACG-BINDING FACTOR (TGA) transcriptional complex to upregulate defense-responsive genes and promote plant resistance against several pathogens, such as the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 and fungal pathogen Botrytis cinerea. Therefore, this study uncovers a MORC1-mediated immune signaling pathway, in which the CPK5-MORC1-NPR1-TGA module transduces Ca2+ signals, leading to the upregulation of defense genes involved in plant immunity.

Abscisic acid (ABA) suppresses Arabidopsis (Arabidopsis thaliana) seed germination and post-germinative growth. Nitrate stimulates seed germination, but whether it directly regulates ABA signaling and the associated underlying molecular mechanisms remain unknown. Here, we showed that nitrate alleviates the repressive effects of ABA on seed germination independently of the nitric oxide (NO) pathway. Moreover, nitrate attenuates ABA signaling activated by ABSCISIC ACID INSENSITIVE3 (ABI3) and ABI5, two critical transcriptional regulators of the ABA pathway. Mechanistic analyses demonstrated that ABI3 and ABI5 physically interact with the nitrate signaling-related core transcription factor NIN-LIKE PROTEIN 8 (NLP8). After ABA treatment, NLP8 suppresses ABA responses during seed germination without affecting ABA content. Notably, nitrate represses ABA signaling mainly through NLP8. Genetic analyses showed that NLP8 acts upstream of ABI3 and ABI5. Specifically, NLP8 inhibits the transcriptional functions of ABI3 and ABI5, as well as their ABA-induced accumulation. Additionally, NLP8 overexpression largely suppresses the ABA hypersensitivity of mutant plants exhibiting impaired NO biosynthesis or signaling. Collectively, our study reveals that nitrate counteracts the inhibitory effects of ABA signaling on seed germination and provides mechanistic insights into the NLP8-ABI3/ABI5 interactions and their antagonistic relationships in ABA signaling.