Biology subjects

Monteiro, E.

Publications and source records attributed to Monteiro, E..

3 recordsLinked to original sources

bioRxiv2026

Three-dimensional nano-imaging reveals subtle changes in xylem structure in CAD-deficient sorghum

Lignin plays a central role in the formation and function of secondary cell walls in vascular plants. However, the structural consequences of lignin modification for cell wall properties and cellular function in grasses remain poorly understood. Here, we investigated how cinnamyl alcohol dehydrogenase (CAD) deficiency alters vascular cell architecture in Sorghum bicolor, using the brown midrib-6 (bmr6) mutant as a model system. Biochemical and histochemical analyses confirmed altered lignin chemistry in bmr6, including increased incorporation of hydroxycinnamaldehyde residues and reduced tricin levels. We applied ptychographic X-ray computed tomography (PXCT) to quantify the cell wall geometry, in three dimensions, at nanometer-scale resolution. PXCT enabled measurements of wall thickness distribution and lumen shape along tracheary elements. Analyses revealed no significant differences in wall thickness between wild-type and bmr6 plants. However, three-dimensional morphometric descriptors indicated reduced lumen convexity in bmr6, suggesting localized modifications not detectable by conventional two-dimensional imaging. Water flow numerical simulations through PXCT-derived images indicated reduced vessel permeability and simulated hydraulic conductivity in bmr6, suggesting that subtle geometric changes may influence performance. These findings highlight the value of three-dimensional imaging for resolving cell wall organization and provide new insight into the architectural resilience of grass xylem in response to targeted lignin modification. HighlightThree-dimensional X-ray nano-imaging reveals alterations in the cell wall architecture that affect simulated hydraulic performance under reduced CAD activity in sorghum.

plant biology↗

bioRxiv2021

Autonomic and respiratory components of orienting behaviors are mediated by descending pathways originating from the superior colliculus

The ability to discriminate competing, external stimuli, and initiate contextually appropriate behaviors, is a key brain function. Neurons in the deep superior colliculus (dSC) integrate multisensory inputs and activate descending projections to premotor pathways responsible for orienting and attention, behaviors which involve adjustments to respiratory and cardiovascular parameters. However, the neural pathways that subserve the physiological components of orienting are poorly understood. We report that orienting responses to optogenetic dSC stimulation are accompanied by short-latency autonomic, respiratory and electroencephalographic effects in awake rats, closely mimicking those evoked by naturalistic alerting stimuli. Physiological responses were not accompanied by detectable aversion or fear and persisted under urethane anesthesia, indicating independence from emotional stress. Moreover, autonomic responses were replicated by selective stimulation of dSC inputs to a subregion in the ventromedial medulla containing spinally-projecting premotor neurons. This putative disynaptic pathway from the dSC represents a likely substrate for autonomic components of orienting.

neuroscience↗

bioRxiv2020

A2E induces the transactivation of RARs, PPARs and RXRs and its effects are counteracted by norbixin in retinal pigment epithelium cells in vitro

N-retinylidene-N-retinylethanolamine (A2E) plays a central role in age-related macular degeneration (AMD) by inducing apoptosis, angiogenesis and inflammation. It has been proposed that A2E effects are mediated at least partly via the retinoic acid receptor (RAR)-. Here we show that A2E binds and transactivates not only RARs, but also peroxisome proliferator-activated receptors (PPARs) and retinoid X receptors (RXRs). Norbixin, which protects retinal pigment epithelium (RPE) cells against apoptosis induced by combined blue light illumination and A2E exposure, is also a ligand of these nuclear receptors (NRs) but does not induce their transactivation. Norbixin inhibits RXRs and PPARs but enhances RARs transactivation induced by A2E. Norbixin also inhibits PPAR-{gamma} transactivation induced by its high affinity ligand troglitazone. Photoprotection of RPE cells by norbixin correlates with maintained levels of the antiapoptotic B-cell lymphoma 2 (Bcl2) protein. Moreover, norbixin reduces protein kinase B (AKT) phosphorylation, NF-{kappa}B and activator protein 1 (AP-1) transactivation, and the mRNA expression of the inflammatory interleukins (IL) 6 and 8 and of vascular endothelial growth factor (VEGF) that are enhanced by A2E. By contrast, norbixin increases matrix metalloproteinase 9 (MMP9) and C-C motif chemokine ligand 2 (CCL2) mRNA expression but has neither effect on extracellular signal-regulated kinase (ERK) phosphorylation, nor on IL-18 mRNA expression in response to A2E. Altogether, we show for the first time that A2E deleterious biological effects appear to be mediated through RARs, PPARs and RXRs. Moreover, we report that the modulation of these NRs by norbixin may open new avenues for the treatment of AMD.

cell biology↗