THESEUS1 modulates cell wall stiffness and abscisic acid production in Arabidopsis thaliana

Plant cells can be distinguished from animal cells by their cell walls and high-turgor pressure. Although changes in turgor and the stiffness of cell walls seem coordinated, we know little about the mechanism responsible for coordination. Evidence has accumulated that plants, like yeast, have a dedicated cell wall integrity maintenance mechanism. It monitors the functional integrity of the wall and maintains integrity through adaptive responses induced by cell wall damage arising during growth, development, and interactions with the environment. These adaptive responses include osmosensitive induction of phytohormone production, defense responses, as well as changes in cell wall composition and structure. Here, we investigate how the cell wall integrity maintenance mechanism coordinates changes in cell wall stiffness and turgor in Arabidopsis thaliana. We show that the production of abscisic acid (ABA), the phytohormone-modulating turgor pressure, and responses to drought depend on the presence of a functional cell wall. We find that the cell wall integrity sensor THESEUS1 modulates mechanical properties of walls, turgor loss point, ABA biosynthesis, and ABA-controlled processes. We identify RECEPTOR-LIKE PROTEIN 12 as a component of cell wall integrity maintenance–controlling, cell wall damage–induced jasmonic acid (JA) production. We propose that THE1 is responsible for coordinating changes in turgor pressure and cell wall stiffness.

On the Biochemical and Physiological Responses of ‘Crimson Seedless’ Grapes Coated with an Edible Composite of Pectin, Polyphenylene Alcohol, and Salicylic Acid

The ‘Crimson seedless’ grape encountered several difficulties during shelf life, including weight loss, rachis browning, and berry shattering. The effect of exogenous pectin (PE) and polyphenol alcohol (PVA) with supporting salicylic acid (SA) at different concentrations (0, 1, and 2 mM) was applied. The coating was applied to bunches for 5 min and stored at room temperature (26 ± 1 °C and RH 65 ± 3%) for 4 days. In this study, postharvest application of PE + PVA-SA can significantly reduce the cell wall degradation enzyme activities of ‘Crimson seedless’ grape during shelf life. ‘Crimson seedless’ bunches, treated with PE + PVA-SA 2 mmol L−1, had a lowered rachis browning index (RB index), weight loss (WL%), and berry shattering percentage (BS%) and preserved berry color hue angle (ho) compared to untreated bunches during shelf-life duration. Moreover, the PE + PVA-SA 2 mM improved berry firmness (BF) and removal force (BRF). It also improved the soluble solid content (SSC%), titratable acidity (TA%), and SSC: TA-ratio, for assessing berry maturity. The cellular metabolism enzyme activities (CMEAs) of the cell wall such as polygalacturonase (PG), cellulase (CEL), xylanase (XYL), and pectinase (PT) were minimized by applying PE + PVA-SA 2 mM coatings throughout storage duration. The accumulation of malondialdehyde (MDA) and cell wall damage, as well as the electrolyte leakage percentage (EL%), was reduced. PE + PVA-SA 2 mM maintained DPPH radical quenching activities and minimized O2− and H2O2 production rates. Collectively, these findings suggest that PE + PVA with the presence of SA as a coating treatment preserved ‘Crimson seedless’ bunches during shelf life. PE + PVA-SA 2 mM might be at least partially ascribed to the enhancement of bunches’ quality traits as well as inhibiting cell wall damage during the shelf-life period.

With an Ear up Against the Wall: An Update on Mechanoperception in Arabidopsis.

Cells interpret mechanical signals and adjust their physiology or development appropriately. In plants, the interface with the outside world is the cell wall, a structure that forms a continuum with the plasma membrane and the cytoskeleton. Mechanical stress from cell wall damage or deformation is interpreted to elicit compensatory responses, hormone signalling, or immune responses. Our understanding of how this is achieved is still evolving; however, we can refer to examples from animals and yeast where more of the details have been worked out. Here, we provide an update on this changing story with a focus on candidate mechanosensitive channels and plasma membrane-localized receptors.

Micafungin-Induced Cell Wall Damage Stimulates Morphological Changes Consistent with Microcycle Conidiation in Aspergillus nidulans

Fungal cell wall receptors relay messages about the state of the cell wall to the nucleus through the Cell Wall Integrity Signaling (CWIS) pathway. The ultimate role of the CWIS pathway is to coordinate repair of cell wall damage and to restore normal hyphal growth. Echinocandins such as micafungin represent a class of antifungals that trigger cell wall damage by affecting synthesis of β-glucans. To obtain a better understanding of the dynamics of the CWIS response and its multiple effects, we have coupled dynamic transcriptome analysis with morphological studies of Aspergillus nidulans hyphae in responds to micafungin. Our results reveal that expression of the master regulator of asexual development, BrlA, is induced by micafungin exposure. Further study showed that micafungin elicits morphological changes consistent with microcycle conidiation and that this effect is abolished in the absence of MpkA. Our results suggest that microcycle conidiation may be a general response to cell wall perturbation which in some cases would enable fungi to tolerate or survive otherwise lethal damage.

Micafungin-induced Cell Wall Damage Stimulates Microcycle Conidiation in Aspergillus nidulans

Fungal cell wall receptors relay messages about the state of the cell wall to the nucleus through the Cell Wall Integrity Signaling (CWIS) pathway. The ultimate role of the CWIS pathway is to coordinate repair of cell wall damage and to restore normal hyphal growth. Echinocandins such as micafungin represent a class of antifungals that trigger cell wall damage by affecting synthesis of beta-glucans, filamentous fungal response to these antifungals are fundamentally unknown. To obtain a better understanding of the dynamics of the CWIS response and its multiple effects, we have coupled dynamic transcriptome analysis with morphological studies of Aspergillus nidulans hyphae responding to micafungin. Our results reveal that expression of the master regulator of asexual development, BrlA, is induced by micafungin exposure. Further study showed that micafungin elicits microcycle conidiation in a BrlA-dependent manner, and that this response is abolished in the absence of MpkA. Our results suggest that microcycle conidiation may be a general response to cell wall perturbation which in some cases would enable fungi to tolerate or survive otherwise lethal damage.

Efg1 and Cas5 Orchestrate Cell Wall Damage Response to Caspofungin in Candida albicans

Echinocandins are recommended as the first-line drugs for the treatment of systemic candidiasis. Cas5 is a key transcription factor involved in the response to cell wall damage induced by echinocandins. Here, through a genetic screen, we report the identification of a second transcription factor Efg1 that is also crucial for proper transcriptional responses to echinocandins. Like CAS5, deletion of EFG1 confers hypersensitivity to caspofungin. Efg1 is required for the induction of CAS5 in response to caspofungin. However, ectopically expressed CAS5 cannot rescue the growth defect of efg1 mutant in caspofungin-containing medium. Deleting EFG1 in the cas5 mutant exacerbates the cell wall stress upon caspofungin addition and renders caspofungin-resistant Candida albicans responsive to treatment. Genome-wide transcription profiling of efg1/efg1 and cas5/cas5 using a RNA-Seq indicates that Efg1 and Cas5 co-regulate numbers of caspofungin-responsive genes expression, but they also independently control some genes induction. We further show that Efg1 interacts with Cas5 by yeast two-hybrid and in vivo immunoprecipitation in the presence or absence of caspofungin. Importantly, Efg1 and Cas5 bind to some caspofungin-responsive genes promoter to coordinately activate their expression. Thus, we demonstrate that Efg1, together with Cas5, controls the transcriptional response to cell wall stress induced by caspofungin.