SUMMARY Jasmonic acid (JA) and salicylic acid (SA) regulate stomatal closure, preventing pathogen invasion into plants. However, to what extent abscisic acid (ABA), SA and JA interact, and what the roles of SA and JA are in stomatal responses to environmental cues, remains unclear. Here, by using intact plant gas‐exchange measurements in JA and SA single and double mutants, we show that stomatal responsiveness to CO2, light intensity, ABA, high vapor pressure deficit and ozone either did not or, for some stimuli only, very slightly depended upon JA and SA biosynthesis and signaling mutants, includingdde2, sid2, coi1,jai1,myc2andnpr1alleles. Although the stomata in the mutants studied clearly responded to ABA, CO2, light and ozone, ABA‐triggered stomatal closure innpr1‐1was slightly accelerated compared with the wild type. Stomatal reopening after ozone pulses was quicker in thecoi1‐16mutant than in the wild type. In intact Arabidopsis plants, spraying with methyl‐JA led to only a modest reduction in stomatal conductance 80 min after treatment, whereas ABA and CO2induced pronounced stomatal closure within minutes. We could not document a reduction of stomatal conductance after spraying with SA. Coronatine‐induced stomatal opening was initiated slowly after 1.5–2.0 h, and reached a maximum by 3 h after spraying intact plants. Our results suggest that ABA, CO2and light are major regulators of rapid guard cell signaling, whereas JA and SA could play only minor roles in the whole‐plant stomatal response to environmental cues in Arabidopsis andSolanum lycopersicum(tomato).
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This content will become publicly available on June 30, 2026
Impaired trap closure in the counting-deficient Venus flytrap mutant DYSCALCULIA is caused by cell wall biomechanics
Abstract Living in nutrient-poor environments, the carnivorous Venus flytrapDionaea muscipulacaptures animal prey to compensate for this deficiency. Stimulation of trigger hairs located on the inner trap surface elicits an action potential (AP). While two consecutive APs result in fast trap closure in wildtype (WT) plants, sustained AP generation by the insect struggling to escape the trap leads to jasmonic acid (JA) biosynthesis, formation of the digestive “stomach”, and release of enzymes needed to decompose the victim. TheDionaea muscipulaDYSCALCULIA (DYSC) mutant is able to fire touch-induced APs, but unlike WT plants, it does not snap-close its traps after two consecutive APs. Moreover, DYSC plants fail to properly initiate the JA pathway in response to mechanostimulation and even wounding, a well-known JA-dependent process conserved among plants. As demonstrated in previous studies, this DYSC mutant defect is associated with impaired decoding of mechanostimulation (i.e. touch) -induced Ca2+signals. External JA application to the trap, however, restores slow trap closure and digestive gland function in DYSC, while rapid trap closure is JA-independent and cannot be rescued by exogenous JA application. Higher frequency mechanostimulation and thus more APs, however, revealed that DYSC is still able to close its traps, albeit much slower than WT plants. To reveal the molecular underpinnings of DYSC’s delayed trap movement, we generated a chromosome-scaleDionaeagenome assembly and profiled gene expression. The refined transcriptomic analysis uncovered widespread misregulation of cell wall-related genes in DYSC, implicating altered cell wall plasticity in the sluggish mutant. Cell indentation studies by atomic force microscopy revealed a strictly localized and strikingly enhanced stiffening of the cell wall for DYSC that may hinder rapid trap closure and snap buckling. Together, these genomic, transcriptomic, and biophysical data identify cell wall elasticity as a key constraint on voltage and Ca2+dependent trap kinetics. This finding documents the interrelationship between mechanosensing and Ca2+signaling in the ultrafast capture organ of the Venus flytrap.
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- Award ID(s):
- 2030871
- PAR ID:
- 10636594
- Publisher / Repository:
- bioRxiv
- Date Published:
- Format(s):
- Medium: X
- Institution:
- bioRxiv
- Sponsoring Org:
- National Science Foundation
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