Biology subjects

Boccaccini, A.

Publications and source records attributed to Boccaccini, A..

4 recordsLinked to original sources

bioRxiv2026

PIEZO1 upregulation in spinal cord astrocytes during MOG 35-55 -induced EAE correlates with ECM remodeling

BackgroundExtracellular matrix (ECM) remodeling is increasingly recognized as an important component of neuroinflammatory pathology in multiple sclerosis (MS), yet the mechanisms by which CNS cells sense and respond to alterations in their mechanical environment and the spatial across which mechanical changes can influence cellular behavior remain poorly understood. Piezo1 is a mechanosensitive ion channel that regulates cellular responses to mechanical stimuli and has recently emerged as a potential modulator of neuroinflammation. MethodsExperimental autoimmune encephalomyelitis (EAE) was induced in C57BL/6 wildtype mice using myelin oligodendrocyte glycoprotein (MOG):35-55. Immunohistochemical analyses were performed in spinal cord gray matter (GM), normal-appearing white matter (NAWM), and white matter lesion (LES) regions to assess ECM remodeling, total Piezo1 expression, and astrocyte-specific Piezo1 expression during acute and chronic EAE stages. Correlations with clinical EAE severity were determined. In parallel, mixed primary murine glial cultures were exposed to substrates of different stiffness and analyzed by transcriptomic profiling to investigate mechanobiological responses in vitro. ResultsECM-associated proteins, including glial fibrillary acidic protein (GFAP), fibronectin-1 and matrix metalloproteinase-3 (MMP3), were regionally upregulated during EAE, indicating widespread tissue remodeling beyond focal inflammatory lesions. Total Piezo1 expression was increased within lesions and transiently elevated in GM, whereas astrocyte-specific Piezo1 remained persistently upregulated during both acute and chronic EAE. Astrocytic Piezo1 expression correlated closely with ECM remodeling and clinical EAE severity, particularly in GM and NAWM. Notably, both total and astrocyte-specific Piezo1 showed stronger associations with clinical disability than classical inflammatory markers. Transcriptomic analysis revealed pronounced stiffness-dependent responses in glial cells, including alterations in extracellular matrix organization, cytokine signaling, cell adhesion, and proliferative pathways. ConclusionsOur findings identify astrocytic Piezo1 as a prominent component of neuroinflammatory tissue remodeling during EAE. The close association of Piezo1 with ECM alterations, clinical disease severity, and stiffness-dependent glial responses supports a link between neuroinflammation and mechanosensory signaling. These results highlight mechanosensation as a potentially important contributor to CNS pathology and establish Piezo1 alteration as a candidate biomarker for neuroinflammatory disease.

Cell Biology↗

bioRxiv2025

Early Flowering 3 (ELF3) inhibits hypocotyl phototropism in light-grown Arabidopsis seedlings.

Phototropic bending of plants towards a light source allows them to position their photosynthetic tissues to optimize light capture. In light-grown (deetiolated) Arabidopsis seedlings, phototropic bending of the hypocotyl is inhibited by light with a high red:far-red ratio (HRFR) and high levels of blue light (HBL). This occurs via activation of the phytochrome B (phyB) and cryptochrome 1 (cry1) photoreceptor signaling pathways. Both phyB and cry1 act upstream of PHYTOCHROME INTERACTING FACTOR (PIF) transcription factors, which are required for hypocotyl bending in light-grown seedlings. Presently, it is not known whether other pathways are involved in the inhibition of PIF-mediated phototropism in light-grown seedlings. To address this, we conducted a screen to identify mutants with increased phototropic bending relative to wild type in HRFR+HBL conditions. Through this screen, we identified EARLY FLOWERING 3 (ELF3), a member of the Evening Complex (EC), as a key inhibitor of phototropic bending in green seedlings. We show that both ELF3 and LUX, another component of the EC, inhibit phototropic bending upstream of PIF4/PIF5. Furthermore, we show that phototropic bending in Arabidopsis seedlings is subject to circadian regulation in an ELF3-dependent manner. Finally, we provide evidence that ELF3 in the grass Brachypodium distachyon also affects phototropism but in an opposite way than in Arabidopsis. One sentence summaryELF3 inhibits hypocotyl phototropism in de-etiolated seedlings growing in favorable light conditions.

plant biology↗

bioRxiv2025

Transcriptional Dynamics and Chromatin Accessibility in the Regulation of Shade-Responsive Genes in Arabidopsis

Open chromatin regions host DNA regulatory motifs that are accessible to transcription factors and the transcriptional machinery. In Arabidopsis, responses to light are heavily regulated at the transcriptional level. Shade, for example, can limit photosynthesis and is rapidly perceived by phytochromes as a reduction of red to far-red light ratio (LRFR). Under shade, phytochromes become inactive, enabling PHYTOCHROME INTERACTING FACTORs (PIFs), particularly PIF7, to promote genome-wide reprogramming essential for LRFR responses. An initial strong and fast regulation of shade-responsive genes is followed by attenuation of this response under prolonged shade. We wanted to determine whether the transcriptional response to shade depends on chromatin accessibility. For this, we used ATAC-seq to profile the chromatin of seedlings exposed to short (1h) and long (25h) simulated shade. We found that PIF7 binding sites were accessible for most early target genes before LRFR treatment. The transcription pattern of most acute shade-responsive genes correlated with a rapid increase in PIF levels and chromatin association at 1h, and its decrease at 25h of shade exposure. For a small subset of acutely responding genes, PIFs also modulate chromatin accessibility at their binding sites early and/or late in the response to shade. Our results suggest that in seedlings a state of open chromatin conformation allows PIFs to easily access and recognize their binding motifs, rapidly initiating gene expression triggered by shade. This transcriptional response primarily depends on a transient increase in PIF stability and gene occupancy, accompanied by changes in chromatin accessibility in a minority of genes.

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↗