Biology subjects

Johanna, K.

Publications and source records attributed to Johanna, K..

4 recordsLinked to original sources

bioRxiv2026

Photosynthesis-derived carbon gates cell cycle activation to enable hormone-autonomous shoot regeneration

Shoot regeneration is a powerful model for cell fate reprogramming but how it occurs in nature remains poorly understood because studies in Arabidopsis thaliana conventionally rely on in vitro assays supplemented with exogenous hormones and sugars. In this study, we established the Hormone-autonomY Direct Regeneration Assay (HYDRA) in which removal of the shoot apical meristem (SAM) initiates shoot regeneration from the cotyledon-hypocotyl boundary domain without hormone or sugar supplementation. We show that photosynthesis-derived carbon and the boundary domain are two separable but convergent requirements for shoot regeneration in HYDRA. Carbon availability increases in the boundary domain where it activates cell cycle progression via the RETINOBLASTOMA-RELATED1 (RBR1) pathway. Carbon deprivation blocks regeneration despite induction of SAM marker genes, indicating that carbon-dependent cell cycle activation is a limiting factor for regeneration. In parallel, perturbation of the boundary domain or its regulators reduces regeneration despite sufficient carbon, indicating that boundary domain identity is independently required. Additionally, exogenous carbon supply overcomes the requirement for SAM removal to induce shoot formation, indicating that carbon availability also acts as an initiation cue. Together, this study reveals an inherent capacity for hormone-autonomous shoot regeneration and identifies photosynthesis-derived carbon as a central regulator of this process.

Plant Biology↗

bioRxiv2022

Abscisic Acid modulates neighbor proximity-induced leaf hyponasty in Arabidopsis

Leaves of shade avoiding plants like Arabidopsis thaliana change their growth pattern and position in response to a low red to far-red ratio (LRFR) that is encountered in dense plant communities. In LRFR, transcription factors of the phytochrome interacting family (PIFs) are de-repressed. PIFs induce auxin production, which is required to promote leaf hyponasty thereby favoring access to unfiltered sunlight. Abscisic acid (ABA) has also been implicated in the control of leaf hyponasty. In addition, gene expression patterns suggest that LRFR regulates the ABA response. Here we show that, in leaves, LRFR leads to a rapid increase in ABA levels. Changes in ABA levels depend on PIFs, which regulate the expression of genes encoding isoforms of the enzyme catalyzing a rate-limiting step in ABA biosynthesis. Interestingly, ABA biosynthesis and signaling mutants have more erect leaves in white light but respond less to LRFR. Consistent with this, ABA application decreases the leaf angle in white light but this response is inhibited in LRFR. Tissue-specific interference with ABA signaling indicates that an ABA response is required in different cell types for LRFR-induced hyponasty. Collectively, our data indicate LRFR triggers rapid PIF-mediated ABA production. ABA plays a different role in controlling hyponasty in white light compared to LRFR. Moreover, ABA exerts its activity in multiple cell types to control leaf position. One sentence summaryAbscisic acid biosynthesis and signaling are required to promote leaf hyponasty in response to a drop in the red to far-red ratio.

plant biology↗

bioRxiv2021

Reduced light access promotes hypocotyl growth via autophagy-mediated recycling

Plant growth ultimately depends on fixed carbon, thus the available light for photosynthesis. Due to canopy light absorption properties, vegetative shade combines reduced light and a low red to far-red ratio (LRFR). In shade-avoiding plants, these two conditions independently promote growth adaptations to enhance light access. However, how these conditions, differing in photosynthetically-available light, similarly promote growth remains unknown. Here, we show that Arabidopsis seedlings adjust metabolism according to light conditions to supply resources for hypocotyl growth enhancement. Transcriptome analyses indicate that reduced light induces starvation responses, suggesting a switch to a catabolic state to promote growth. Accordingly, reduced light promotes autophagy. In contrast, LRFR promotes anabolism including biosynthesis of plasma-membrane sterols downstream of PHYTOCHROME-INTERACTING FACTORs (PIFs) acting in hypocotyls. Furthermore, sterol biosynthesis and autophagy are indispensable for shade-induced hypocotyl growth. We conclude that vegetative shade enhances hypocotyl growth by combining autophagy-mediated recycling and promotion of specific anabolic processes. HIGHLIGHTSO_LIReduced light and LRFR induce catabolism and anabolism, respectively C_LIO_LIReduced light promotes autophagy to enhance hypocotyl growth in vegetative shade C_LIO_LILRFR enhances hypocotyl growth by promoting plasma membrane lipid biosynthesis C_LIO_LIIn LRFR, PIFs promote sterol biosynthesis specifically in the hypocotyl C_LI

plant biology↗

bioRxiv2020

In Arabidopsis, low blue light enhances phototropism by releasing cryptochrome 1-mediated inhibition of PIF4 expression

Shade-avoiding plants including Arabidopsis thaliana display a number of growth responses elicited by shade cues including elongation of stem-like structures and repositioning of leaves. Shade also promotes phototropism of de-etiolated seedlings through repression of phytochrome B (phyB) presumably to enhance capture of unfiltered sunlight. Light cues indicative of shade include a reduction in the blue and red portions of the solar spectrum and a low red to far-red ratio. Here we show that in Arabidopsis seedlings both low blue and a low red to far-red ratio are required to rapidly enhance phototropism. However, prolonged low blue treatments through reduced cryptochrome 1 (cry1) activation are sufficient to promote phototropism. The enhanced phototropic response of cry1 mutants in the lab and in response to natural canopies depends on PHYTOCHROME INTERACTING FACTORs (PIFs). In favorable light conditions, cry1 limits the expression of PIF4 while in low blue light PIF4 expression increases, which contributes to phototropic enhancement. The analysis of a quantitative DII auxin reporter indicates that low blue light leads to enhanced auxin levels in the hypocotyl and, upon phototropic stimulation, a steeper auxin gradient across the hypocotyl. We conclude that phototropic enhancement by canopy shade results from the combined activities of phytochrome B and cry1 that converge on PIF regulation. ONE SENTENCE SUMMARYThe persistent depletion of blue light in natural canopy shade relieves the inhibitory effect of cryptochrome 1 on PIF4, enhancing phototropism in de-etiolated Arabidopsis seedlings. Financial supportThis work was supported by the University of Lausanne and a grant from the Swiss National Science foundation (n{degrees} 310030B_179558 to C.F.); Human Frontier Science Program organization (HFSP) Grant RPG0054-2013, ANR-12-BSV6-0005 grant (AuxiFlo) to T.V.; The University of Buenos Aires (Grant 20020100100437 to J. J. C.), and Agencia Nacional de Promocion Cientifica y Tecnologica of Argentina (Grant PICT-2018-01695 to J. J. C.). Alessandra Boccaccini and Martina Legris are funded by Marie Curie fellowships H2020-MSCA-IF-2017 grants CRoSh 796283 and Flat-Leaf 796443 respectively.

plant biology↗