A nonproteinaceous Fusarium cell wall extract triggers receptor-like protein-dependent immune responses in Arabidopsis and cotton.

Fusarium wilt caused by the ascomycete fungus Fusarium oxysporum is a devastating disease of many economically important crops. The mechanisms underlying plant responses to F. oxysporum infections remain largely unknown. We demonstrate here that a water-soluble, heat-resistant and nonproteinaceous F. oxysporum cell wall extract (FoCWE) component from multiple F. oxysporum isolates functions as a race-nonspecific elicitor, also termed pathogen-associated molecular pattern (PAMP). FoCWE triggers several demonstrated immune responses, including mitogen-activated protein (MAP) kinase phosphorylation, reactive oxygen species (ROS) burst, ethylene production, and stomatal closure, in cotton and Arabidopsis. Pretreated FoCWE protects cotton seeds against infections by virulent F. oxysporum f. sp. vasinfectum (Fov), and Arabidopsis plants against the virulent bacterium, Pseudomonas syringae, suggesting the potential application of FoCWEs in crop protection. Host-mediated responses to FoCWE do not appear to require LYKs/CERK1, BAK1 or SOBIR1, which are commonly involved in PAMP perception and/or signalling. However, FoCWE responses and Fusarium resistance in cotton partially require two receptor-like proteins, GhRLP20 and GhRLP31. Transcriptome analysis suggests that FoCWE preferentially activates cell wall-mediated defence, and Fov has evolved virulence mechanisms to suppress FoCWE-induced defence. These findings suggest that FoCWE is a classical PAMP that is potentially recognised by a novel pattern-recognition receptor to regulate cotton resistance to Fusarium infections.

Identification of Players Controlling Meristem Arrest Downstream of the FRUITFULL-APETALA2 Pathway.

The end of the reproductive phase in monocarpic plants is determined by a coordinated arrest of all active meristems, a process known as global proliferative arrest (GPA). GPA is linked to the correlative control exerted by developing seeds and, possibly, the establishment of strong source-sink relationships. It has been proposed that the meristems that undergo arrest at the end of the reproductive phase behave at the transcriptomic level as dormant meristems, with low mitotic activity and high expression of abscisic acid response genes. Meristem arrest is also controlled genetically. In Arabidopsis (Arabidopsis thaliana), the MADS-box transcription factor FRUITFULL induces GPA by directly repressing genes of the APETALA2 (AP2) clade. The AP2 genes maintain shoot apical meristem (SAM) activity in part by keeping WUSCHEL expression active, but the mechanisms downstream of this pathway remain elusive. To identify target genes, we performed a transcriptomic analysis, inducing AP2 activity in meristems close to arrest. Our results suggest that AP2 controls meristem arrest by repressing genes related to axillary bud dormancy in the SAM and negative regulators of cytokinin signaling. In addition, our analysis indicates that genes involved in the response to environmental signals also respond to AP2, suggesting that it could modulate the end of flowering by controlling responses to both endogenous and exogenous signals. Our results support the previous observation that at the end of the reproductive phase the arrested SAM behaves as a dormant meristem, and they strongly support AP2 as a master regulator of this process.