Journal of Integrative Plant Biology最新文献

This commentary on Wang et al. (2025) and Phan et al. (2025) highlights previously undiscovered Xanthomonas pathways for nutrition acquisition, explains how Xanthomonas bacteria hijack host molecular machinery through their effector proteins, and discusses how these studies can be used to develop new disease resistance mechanisms.

Acid-producing fungal pathogens like Valsa mali enhance infectivity by secreting organic acids to acidify host environments, though the underlying cellular pH manipulation mechanisms remain unclear. Here, we identified VmAGP1 as a V. mali virulence factor whose knockout reduces virulence while heterologous expression in apples increases susceptibility. Using yeast two-hybrid (Y2H), bimolecular fluorescence complementation (BiFC), and co-immunoprecipitation (Co-IP) assays, we demonstrated that VmAGP1 interacts with apple receptor-like kinase MdLecRK2, which negatively regulates disease resistance. VmAGP1 promotes MdLecRK2 homo-dimerization, confirmed by luciferase complementation imaging (LCI) and Co-IP. Further studies reveal that MdLecRK2 interacts with and phosphorylates vacuolar H⁺-ATPase MdVHAc"1, which also negatively regulates resistance. Flow cytometry shows that VmAGP1 expression lowers intracellular pH in apple protoplasts, further decreased by MdLecRK2/MdVHAc"1 overexpression. We conclude that V. mali secretes VmAGP1 to induce MdLecRK2 homo-dimerization, triggering a phosphorylation cascade with MdVHAc"1 that acidifies apple cells to facilitate infection. This study reveals a novel pH manipulation strategy in V. mali pathogenesis, identifying potential targets for controlling Apple Valsa canker.

Seed weight is a pivotal yield-determining trait in crops, and yet, the genetic and molecular mechanisms underlying its regulation in polyploid species remain underexplored. In a previous study, we identified cqSW.A03-2, a QTL that regulates thousand seed weight (TSW) in rapeseed (Brassica napus). Here, we identify BnaA3.AHK2, encoding a histidine kinase, as the causal gene of cqSW.A03-2. BnaA3.AHK2 enhances TSW through maternal control of seed coat cell expansion without significantly compromising other yield-related traits. Protein sequence divergence between parental haplotypes caused functional differentiation, with only the ZY50 allele showing functional kinase activity and rescuing developmental defects in Arabidopsis cytokinin receptor mutants. Strikingly, BnaA3.AHK2 seems to be a cytokinin-independent operator, contrasting with the canonical cytokinin signaling pathway. Transcriptome and protein interaction analyses reveal a signaling module where BnaA3.AHK2 engages BnaAHP-BnaARR phosphorelay components to regulate downstream targets. Notably, the favorable cqSW.A03-2 haplotype has been historically selected in modern breeding, and its introgression into elite hybrids boosted TSW by 3.6%-9.1%, demonstrating its breeding value. Our findings unveil a non-canonical signaling pathway for seed size regulation, providing a strategic genetic target to break yield trade-offs in polyploid crops.

In poplar trees, a molecular switch involving phytochrome B and PHYTOCHROME-INTERACTING FACTOR 4 responds to cool temperatures by keeping growth active, preventing premature dormancy. This mechanism, which differs from that in Arabidopsis, helps trees adapt to cool summers and ensures survival in seasonal environments.

While plant salicylic acid (SA) signaling via NPR1-PR1 is well-characterized in pathogen resistance, its role against piercing-sucking insects remains unclear in rice. Here, we demonstrate that leafhopper infestation in rice induces SA-mediated resistance, which defends against insect infestation via pathogenesis-related protein OsPR1a. However, prolonged infestation triggers autophagy-dependent degradation of OsPR1a through its interaction with OsATG8b, fine-tuning immunity to prevent excessive defense activation. Strikingly, this autophagy-mediated OsPR1a degradation represents a conserved regulatory mechanism in rice during brown planthopper infestation. A rice rhabdovirus in leafhopper vectors secretes glycoprotein on virion envelopes to rice phloem, where it binds OsATG6b and OsPR1a to enhance autophagic OsPR1a turnover, ultimately facilitating insect vector feeding and viral transmission by leafhopper vectors. Our work reveals an adaptive mechanism by which a vector-borne virus hijacks plant autophagy to evade SA immunity, highlighting OsPR1a as a critical convergence point in plant-insect-virus interactions.

This commentary highlights emerging strategies for efficient plant regeneration through control of morphogenic regulators that govern cell identity. Synthetic expression systems, enabled by high-throughput discovery platforms, can direct plant cells to form new tissues or organs, opening new possibilities for efficient genetic engineering of agronomically important crops.

Global warming imposes a major threat to plant survival by disrupting growth homeostasis, yet plants adapt to elevated temperatures through thermomorphogenesis. Although auxin signaling is known to orchestrate these adaptive responses, how temperature perception is integrated with auxin remains poorly understood. Here, we identify the CrRLK1L-family receptor kinase FERONIA (FER) as a central regulator of thermomorphogenesis in Arabidopsis thaliana. Under warm-temperature conditions, FER undergoes proteolytic cleavage, releasing its cytosolic domain FER^CD, which translocates into the nucleus via an importin-dependent pathway. Once in the nucleus, FER^CD phosphorylates the non-canonical AUX/IAA protein IAA29, thereby relieving its inhibition of ARF19 and promoting hypocotyl elongation. Transcriptomic analyses further reveal that FER and ARF19 co-regulate thermo-inducible genes involved in auxin signaling and cell wall remodeling. Together, these findings uncover the mechanism by which FER integrates thermal cues through proteolytic activation and phosphorylation-dependent modulation of auxin signaling, establishing a new paradigm for receptor kinase-mediated environmental adaptation in plants.

CRISPR/Cas12i3 belongs to the type V-I Cas system, characterized by its smaller protein size and less restricted canonical "TTN" protospacer adjacent motif. Developments of Cas12i3-mediated base editing systems for either C-to-T or A-to-G transitions will expand the editing scope and enrich the plant base editing toolkits for crop improvement. However, while the Cas12i3-based cytosine base editor (CBE) only shows very low editing efficiency in plants, its adenine base editor (ABE) has not been documented as yet. Here, we engineered a series of Cas12i3 (5M)-based CBEs (V0-V5) and ABEs (V0-V5) by fusing a deactivated dCas12i3 (5M) with a transactivation module VP64, a single-stranded DNA-binding domain Rad51, or a double-stranded DNA-binding domain HMG-D, or in combinations, and systemically evaluated their performance in rice protoplasts. Our results demonstrated that synergistic combinations of both VP64 and HMG-D outperformed other architectures and significantly boosted the efficiencies of Cas12i3 (5M)-based CBE and ABE for C-to-T and A-to-G base editing and expanded the editing window. In stable lines, in comparison to the non-fusion control, the optimized Cas12i3 (5M)-based CBE-V5 and ABE-V5 enabled up to 4.78- and 3.35-fold higher editing efficiencies, with the maximum C-to-T and A-to-G efficiencies reaching 32.35% and 38.24%, respectively, and a higher proportion of homozygous mutants in the T₀ generation. Furthermore, we generated herbicide-resistant rice germplasm by using CBE-V5 and ABE-V5, demonstrating their potential for precision breeding in crops. Together, here, we report novel Cas12i3 (5M)-based CBE and ABE that substantially enrich base editing toolkits for improvement of rice and potentially other crops.

Small G proteins, functioning as monomeric GTPases, are critical molecular switches that regulate diverse processes in plants. However, little is known about their protein homeostasis during immune responses. Here, we demonstrate that OsRab11C1, encoding a Rab-type GTPase, is transcriptionally upregulated upon Magnaporthe oryzae infection. Strikingly, loss of OsRab11C1 enhances rice blast resistance, concomitant with increased defense gene expression, MAPK activation, and ROS burst. Mechanistically, we identify the E3 ubiquitin ligase EL5 as an interactor that ubiquitinates and targets OsRab11C1 for degradation via the 26S proteasome. Consistently, EL5 acts upstream of OsRab11C1 and positively regulates rice immunity. Further analysis reveals that OsRab11C1 interacts with and stabilizes mitogen-activated protein kinase kinase OsMKK6, thereby facilitating its autophosphorylation activity. In return, OsMKK6 acts as a negative regulator of rice programmed cell death and immunity. Collectively, our findings unveil a dynamic EL5-OsRab11C1-OsMKK6 signaling module that orchestrates rice immunity against pathogen invasion.