Cai-Zhong Jiang

Organ abscission represents a critical adaptive strategy for plant survival, yet the post-translational mechanisms ensuring its irreversible remain poorly understood. Here, we unveil a signaling module, MITOGEN-ACTIVATED PROTEIN KINASE 3 (RhMPK3)-LATERAL ORGAN BOUNDARIES DOMAIN 41 (RhLOB41)-WRKY DNA-BINDING PROTEIN 9 (RhWRKY9), that gates ethylene-induced petal abscission in rose ( Rosa hybrida ) by orchestrating reactive oxygen species (ROS) homeostasis. We demonstrate that the transcription factor RhWRKY9 acts as a dual-function regulator, concurrently activating ROS production via activation of RESPIRATORY BURST OXIDASE HOMOLOGUE D ( RhRBOHD ) and suppressing scavenging via repression of CATALASE 2 ( RhCAT2 ), thereby generating a ROS burst that locks abscission progression. Ethylene primes this process by destabilizing RhLOB41, a transcriptional repressor of RhWRKY9 , through RhMPK3-mediated phosphorylation at Ser30. Phosphorylation creates a phosphodegron that targets RhLOB41 for autophagy-dependent degradation. Our findings redefine ROS as decisive executors of abscission and establish bidirectional ROS control as a paradigm for irreversible developmental transitions.

Summary: Precise control of cell expansion kinetics is fundamental to plant organogenesis. This process requires the dynamic integration of growth‐promoting and growth‐inhibiting signals to maintain morphological homeostasis. While brassinosteroids (BRs) promote growth via the transcription factor BRASSINAZOLE RESISTANT 1 (BZR1), the mechanisms that prevent deregulated overgrowth during rapid expansion remain elusive. We find that RhBZR1 promotes rose ( Rosa hybrida ) petal enlargement by specifically accelerating the rate, rather than prolonging the duration, of cell expansion. Conversely, RhMPK7 functions as a key repressor of petal enlargement. RhMPK7 phosphorylates RhBZR1 at Ser‐173, impairing its DNA‐binding affinity and transcriptional activity; consequently, plants expressing the non‐phosphorylatable Rh BZR1 ^S173A variant display significantly enlarged petals. We further show that ethylene simultaneously activates RhMPK7 and stabilizes the RhMPK7–RhBZR1 interaction. Genetic analyses confirm that RhMPK7 restricts petal expansion specifically by antagonizing RhBZR1, and this module is essential for ethylene‐mediated growth suppression. These results indicate a phosphorylation‐based ‘speed governor’ that dynamically restrains hormone‐induced rapid cell expansion, offering a new paradigm for the posttranslational gating of organ size.

SCIEPublish is an international open-access journal publishing service provider run by SCIE Publishing Limited, dedicated to supporting and inspiring scientists or institutions/societies who aspire to publish high-quality journals.

Gaseous phytohormone ethylene regulates various aspects of plant development. Ethylene is perceived by ER membrane-localized receptors, which are inactivated upon binding with ethylene molecules, thereby initiating ethylene signal transduction. Here, we report that a novel E3 ligase RING finger for Ethylene receptor Degradation (RED) and its E2 partner UBC32 ubiquitinate ethylene-bound receptors for degradation through an ER associated degradation (ERAD) pathway in both Rosa hybrida and Solanum lycopersicum. The depletion of RED or UBC32 leads to hypersensitivity to ethylene, which is manifested as premature leaf abscission and petal shedding in roses, as well as the dwarf plants and accelerated fruit ripening in tomatoes. Disruption of the conserved ethylene binding site of receptors prevents RED-mediated degradation of the receptors. Our study discovers an ERAD branch that facilitates the ethylene-induced degradation of receptors, and provides insights into how the plant’s response to ethylene can be controlled by modulating the turnover of ethylene receptors.

The KNOTTED1-LIKE HOMEOBOX PROTEIN1 (SlKD1) is a master abscission regulator in tomato ( Solanum lycopersicum ). Here, we identified an SlKD1-interacting transcription factor GATA transcription factor 6 (SlGATA6), which is required for maintaining the auxin-response gradient and preventing abscission. SlGATA6 up-regulates the expression of SlLAX2 and SlIAA3 . The AUXIN RESISTANT/LIKE AUXIN RESISTANT (AUX/LAX) proteins SlLAX2-dependent asymmetric auxin distribution causes differential accumulation of Auxin/Indole-3-Acetic Acid 3 (SlIAA3) and its homolog SlIAA32 across different abscission zone cells. It is also required for SUMOylation of AUXIN RESPONSE FACTOR 2a (SlARF2a), a key suppressor of auxin signaling and abscission initiator. Moreover, SlIAA3 and SlIAA32 depress SUMOylated SlARF2a, thus suppressing SlARF2a function. The interaction between SlKD1 and SlGATA6 suppresses SlGATA6 binding to the promoters of SlLAX2 and SlIAA3 , thereby disrupting the auxin-response gradient and triggering abscission. This regulatory mechanism is conserved under low light–induced abscission in diverse Solanaceae plants. Our findings reveal a critical role of SlKD1 in modulating the auxin-response gradient and abscission initiation.

Summary: Temporal decline in microRNA miR156 expression is crucial for the transition to, and maintenance of, the adult phase and flowering competence in flowering plants. However, the molecular mechanisms underlying the temporal regulation of miR156 reduction remain largely unknown. Here, we investigated the epigenetic mechanism regulating the temporal silencing of cin‐MIR156 in wild chrysanthemum (Chrysanthemum indicum), focusing on the role of the lysine‐specific demethylase CiLDL1 and the nuclear factor Y complex. CiLDL1 and CiNF‐YB8 interact with the classical histone‐like fold domain (HFD) of CiNF‐YC1 and CiNF‐YA3, which form distinct heterotrimers binding to the ‘CCAAT’ box in the promoter region of cin‐MIR156ab. CiLDL1 and CiNF‐YB8 have opposing effects on cin‐MIR156ab expression, with influencing histone 3 lysine 4 demethylation (H3K4me2) levels at the cin‐MIR156ab locus. During aging, decreased CiNF‐YB8 expression leads to a quantitative switch from the CiNF‐YA3–CiNF‐YC1–CiNF‐YB8 heterotrimer to the CiNF‐YA3–CiNF‐YC1–CiLDL1 heterotrimer, which reduces H3K4me2 levels at the cin‐MIR156ab locus, thus temporal silencing its expression. Our results thus reveal that the dynamic regulatory shift between CiLDL1 and CiNF‐YB8 ensures proper aging‐dependent flowering in chrysanthemum.

Petunia (Petunia hybrida) plants are highly threatened by a diversity of viruses, causing substantial damage to ornamental quality and seed yield. However, the regulatory mechanism of virus resistance in petunia is largely unknown. Here, we revealed that a member of petunia WRKY transcription factors, PhWRKY30, was dramatically up-regulated following Tobacco rattle virus (TRV) infection. Down-regulation of PhWRKY30 through TRV-based virus-induced gene silencing increased green fluorescent protein (GFP)-marked TRV RNA accumulation and exacerbated the symptomatic severity. In comparison with wild-type (WT) plants, PhWRKY30-RNAi transgenic petunia plants exhibited a compromised resistance to TRV infection, whereas an enhanced resistance was observed in PhWRKY30-overexpressing (OE) transgenic plants. PhWRKY30 affected salicylic acid (SA) production and expression of arogenate dehydratase 1 (PhADT1), phenylalanine ammonia-lyase 1 (PhPAL1), PhPAL2b, nonexpressor of pathogenesis-related proteins 1 (PhNPR1), and PhPR1 in SA biosynthesis and signaling pathway. SA treatment restored the reduced TRV resistance to WT levels in PhWRKY30-RNAi plants, and application of SA biosynthesis inhibitor 2-aminoindan-2-phosphonic acid inhibited promoted resistance in PhWRKY30-OE plants. The protein-DNA binding assays showed that PhWRKY30 specifically bound to the promoter of PhPAL2b. RNAi silencing and overexpression of PhPAL2b led to decreased and increased TRV resistance, respectively. The transcription of a number of reactive oxygen species- and RNA silencing-associated genes was changed in PhWRKY30 and PhPAL2b transgenic lines. PhWRKY30 and PhPAL2b were further characterized to be involved in the resistance to Tobacco mosaic virus (TMV) invasion. Our findings demonstrate that PhWRKY30 positively regulates antiviral defense against TRV and TMV infections by modulating SA content.

In tomato, SlNOR and SlNOR-like1, members of the NAC family of transcription factors (TFs), are known to play critical roles in regulating fruit ripening and are highly expressed in floral organs. However, their role in flower development remains unclear. In this study, we generated and functionally characterized a double knockout mutant, nor/nor-like1. Our findings reveal that the pollen abortion of the nor/nor-like1 impedes ovarian enlargement, resulting in fruit formation failure. Histological analyses demonstrate that the pollen wall collapse occurs during the mature pollen stage and leads to the abnormal pollen wall component deposition at the microspore stage, resulting in the male sterility in the double knockout mutant lines. Kyoto Encyclopedia of Genes and Genomes enrichment pathway analyses further suggest that the loss of SlNOR and SlNOR-like1 function affects several metabolic pathways related to pollen development, including ‘ABC transporters’, ‘lipid metabolism’, ‘phenylpropanoid biosynthesis’, ‘hormone signal transduction’, ‘starch and sucrose metabolism’, and ‘cutin, suberine, and wax biosynthesis’. Furthermore, our results demonstrate that SlNOR and SlNOR-like1 could directly bind to the promoters of key genes associated with pollen wall formation and activate their expression, including ATP-binding cassette transporters of the G family (SlABCG8/9/23), ECERIFERUM (SlCER1), and glycine-rich protein (SlGRP92). These findings suggest that SlNOR and SlNOR-like1 may play a redundant role in the biosynthesis and transport of sporopollenin precursors, cuticular wax biosynthesis, and exine formation. In summary, our study highlights a previously uncharacterized role of SlNOR and SlNOR-like1 in tomato pollen wall formation and male fertility.

Drought stress substantially decreases crop yields by causing flowers and fruits to detach prematurely. However, the molecular mechanisms modulating organ abscission under drought stress remain unclear. Here, we show that expression of CALMODULIN2 (CaM2) is specifically and sharply increased in the pedicel abscission zone in response to drought and plays a positive role in drought-induced flower drop in tomato (Solanum lycopersicum). Due to partial functional redundancy with SlCaM6, we generated the Slcam2 Slcam6 double mutant, which showed minimal flower drop under drought. SlCaM2 and SlCaM6 interacted with the transcription factor signal responsive 3L (SlSR3L), with the 3 proteins operating in the same pathway, based on genetic data. We identified Protease inhibitor26 (SlPI26) as a target gene of SlSR3L by DNA affinity purification sequencing and transcriptome analysis. SlPI26 specifically inhibited the activity of the phytaspase SlPhyt2, hence preventing the generation of active phytosulfokine peptide and negatively regulating drought-induced flower drop. SlCaM2 and SlCaM6 enhanced the repression of SlPI26 expression by SlSR3L, promoting drought-induced flower drop. In addition, the nonphototropic hypocotyl3 (SlNPH3)–Cullin3 (SlCUL3) complex, which relies on auxin, interacted with SlSR3L to induce its degradation. However, under drought conditions, SlNPH3–SlCUL3 function is compromised due to lower auxin concentration. These results uncover a regulatory network that precisely controls floral drop in response to drought stress.