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Kieber, J. J.

Publications and source records attributed to Kieber, J. J..

4 recordsLinked to original sources

Cellulose Synthase Complex and Remorin Nanodomains Mediate Stress Resilience Through Cell Wall-Plasma Membrane Attachments

HighlightsO_LIThe plasma membrane forms attachments to the plant cell wall that are revealed by hyperosmotic shock and correlate with tolerance to stress. C_LIO_LICellulose Synthase Complex (CSC) clusters and REMORIN (REM) nanodomains localize to cell wall-plasma membrane attachment sites. C_LIO_LICSC density at the plasma membrane determines the extent of cell wall-plasma membrane attachment under hyperosmotic stress. C_LIO_LIREMs rapidly form nanodomains under hyperosmotic stress and are associated with SHOU4/4L, CSC exocytosis inhibitors that limit CSC density at the plasma membrane. C_LI The outer cell surface of an organism is the frontline for detecting and responding to environmental stimuli. In plants, this interface consists of the plasma membrane that lies beneath the cell wall and remains associated with it through attachment sites. These wall-membrane attachments become evident upon hyperosmotic shock, when severe water loss causes the membrane to retract from the wall. Despite their long-standing observation, the molecular identity and function of these attachments remain poorly understood. Here, we identified two mechanisms governing wall-membrane attachments: one dependent on the Cellulose Synthase Complex (CSC), whose density at the plasma membrane positively correlates with resistance to hyperosmotic stress, and the other on REMORIN (REM), which acts antagonistically to the CSC mechanism. Using proximity-labeling proteomics, we identified SHOU4/4L as REM-associated proteins that mediate this antagonism. Together, our findings reveal how wall-membrane attachments are patterned to mediate plant cell resilience under water stress.

plant biology↗

1-Aminocyclopropane-1-carboxylic acid oxidase determines the fate of ethylene biosynthesis in a tissue-specific way to fine-tune development and stress resilience

Ethylene is involved in several developmental processes and responses towards (a)biotic stress. In seed plants, ethylene is produced from its precursor 1-aminocyclopropane-1-carboxylic acid (ACC) by the enzyme ACC-oxidase (ACO). Despite its key role in ethylene synthesis, the ACO gene family has not yet been fully characterized. We investigated the five ACO members of Arabidopsis thaliana and revealed a tissue-and developmentally specific expression pattern. Furthermore, the five ACO enzymes each have a different capacity to produce ethylene. Combined, this allows for a precise spatial and temporal regulation of ethylene synthesis. At the sub-cellular level, we uncovered that ACOs reside in the cytosol, where ethylene is likely synthesized, but surprisingly also in the nucleus. Using reverse genetics of single and higher order aco mutants we revealed a high degree of gene redundancy and minimal phenotypes. A lack of ethylene synthesis by knocking out all five ACOs did not impair normal vegetative and generative development but did influence processes associated with high rates of ethylene production such as petal abscission. This suggests that ethylene is not a prime regulator of development, but more a moderator. We also showed that the inability to synthesize ethylene impairs some abiotic (nutrient deficiency and metal toxicity) and biotic (Botrytis cinerea) stress responses, similar as plants insensitive towards ethylene, corroborating the role of ethylene in mediating stress responses. In conclusion, the ACO gene family enables plants to fine-tune their ethylene synthesis rates, but a lack their off is not crucial for normal development and stress survival.

plant biology↗

Ethylene-triggered subcellular trafficking of CTR1 suppresses the response to ethylene gas

Ethylene gas controls plant growth and stress responses. Ethylene-exposed dark-grown seedlings exhibit dramatic growth reduction, yet the seedlings rapidly return to the basal growth rate when ethylene gas is removed. However, the underlying mechanism governing this reversible acclimation of dark-grown seedlings to ethylene remains enigmatic. Here, we report that ethylene triggers the translocation of the Raf-like protein kinase CONSTITUTIVE TRIPLE RESPONSE1 (CTR1), a negative regulator of ethylene signaling, from the endoplasmic reticulum to the nucleus. Nuclear-localized CTR1 stabilizes the ETHYLENE-INSENSITIVE3 (EIN3) transcription factor via interaction with the EIN3-BINDING F-box (EBF) proteins, thus enhancing the ethylene response and delaying growth recovery. These findings uncover a mechanism of the ethylene signaling pathway that links the spatiotemporal dynamics of cellular signaling components to organismal responses.

plant biology↗

EXO70D isoforms mediate selective autophagic degradation of Type-A ARR proteins to regulate cytokinin sensitivity

The phytohormone cytokinin influences many aspects of plant growth and development, several of which also involve the cellular process of autophagy, including leaf senescence, nutrient re-mobilization, and developmental transitions. The Arabidopsis type-A Response Regulators (type-A ARR) are negative regulators of cytokinin signaling that are transcriptionally induced in response to cytokinin. Here, we describe a mechanistic link between cytokinin signaling and autophagy, demonstrating that plants modulate cytokinin sensitivity through autophagic regulation of type-A ARR proteins. Type-A ARR proteins were degraded by autophagy in an AUTOPHAGY-RELATED (ATG)5-dependent manner. EXO70D family members interacted with Type-A ARR proteins, likely in a phosphorylation-dependent manner, and recruited them to autophagosomes via interaction with the core autophagy protein, ATG8. Consistently, loss-of-function exo70D1,2,3 mutants compromised targeting of type-A ARRs to autophagic vesicles, have elevated levels of type-A ARR proteins, and are hyposensitive to cytokinin. Disruption of both type-A ARRs and EXO70D1,2,3 compromised survival in carbon-deficient conditions, suggesting interaction between autophagy and cytokinin responsiveness in response to stress. These results indicate that the EXO70D proteins act as selective autophagy receptors to target type-A ARR cargos for autophagic degradation, demonstrating that cytokinin signaling can be modulated by selective autophagy.

plant biology↗