Biology subjects

Cerri, M.

Publications and source records attributed to Cerri, M..

6 recordsLinked to original sources

bioRxiv2024

Co-cultivation with Azolla affects the metabolome of whole rice plant beyond canonical inorganic nitrogen fertilization

Azolla spp. are floating ferns used for centuries as biofertilizers to enrich the soil with inorganic nitrogen and improve rice yields. In this study, rice plants were grown together with Azolla by maintaining a low and constant concentration of inorganic nitrogen. We employed a combination of non-targeted metabolomics, chemometrics, and molecular networking to dissect the impact of Azolla co-cultivation on the metabolome of rice roots-and leaves. Our analyses revealed that Azolla releases a broad range of metabolites in the culture medium, mainly comprising small peptides and flavonoids. Moreover, in rice co-cultivated with Azolla, we observed a systematic response in the upregulation of metabolites that started from the roots and, over time, shifted to the leaves. During the early stages of co-cultivation, Azolla led to the accumulation of small peptides, lipids, and carbohydrates in roots, and flavonoid glycosides and carbohydrates in leaves of rice. Consistent with these results, transcriptomics analysis of rice roots indicated significant changes in the expression of genes coding for small peptide and lipid transporters, and genes involved in amino acid salvage and biosynthesis. Overall, our study highlights novel growth-promoting effects of Azolla on rice which could facilitate the development of sustainable techniques to increase yields. HighlightsThe aquatic fern Azolla synthesizes and releases a broad range of growth promoting metabolites (i.e. small peptides) that can be absorbed by the roots of co-cultivated rice plants

plant biology↗

bioRxiv2024

Co-cultivating rice plants with Azolla filiculoides modifies root architecture and timing of developmental stages

Strategies for increasing the yield of rice, the staple food for more than half of the global population, are needed to keep pace with the expected worldwide population increase, and sustainably forefront the challenges posed by climate change. In Southern-East Asian countries, rice farming benefits from the use of Azolla spp. for nitrogen supply. In virtue of the symbiosis with the nitrogen-fixing cyanobacterium Trichormus azollae, Azolla spp. are ferns that release nitrogen into the environment upon decomposition of their biomass. However, if and to what extent actively growing Azolla plants impact on the development of co-cultivated rice plantlets remains to be understood. Here, we show that actively growing Azolla filiculoides plants alter the architecture of the roots and accelerates the differentiation and proliferation of leaves and tillers in co-cultivated rice plants. These changes result from an intimate cross-talk between rice and A. filiculoides, in which hormones and other metabolites released by the fern in the growth medium trigger an alteration in the rice root transcriptome and the hormonal profiles of both roots and leaves. Overall, the present data let us argue that co-cultivation with A. filiculoides might prime rice plants to better deal with both abiotic and biotic stress. HighlightAzolla filiculoides alters the root transcriptome and hormonal balance in both roots and leaves of co-cultivated rice plantlets, thereby interfering with the progression of their developmental programs

plant biology↗

bioRxiv2022

Synthetic torpor triggers a neuroprotective and regulated mechanism in the rat brain, leading to the reversibility of Tau protein hyperphosphorylation.

Hyperphosphorylated Tau protein (PPTau) is the hallmark of tauopathic neurodegeneration. During "synthetic torpor" (ST), a transient hypothermic state which can be induced in rats by the local pharmacological inhibition of the Raphe Pallidus, a reversible brain Tau hyperphosphorylation occurs. The aim of the present study was to elucidate the - as yet unknown - molecular mechanisms underlying this process, at both a cellular and systemic level. Different phosphorylated forms of Tau and the main cellular factors involved in Tau phospho-regulation were assessed by western blot in the parietal cortex and hippocampus of rats induced in ST, at either the hypothermic nadir or after the recovery of euthermia. Pro- and anti-apoptotic markers, as well as different systemic factors which are involved in natural torpor, were also assessed. Finally, the degree of microglia activation was determined through morphometry. Overall, the results show that ST triggers a regulated biochemical process which can counteract PPTau formation starting, unexpectedly even for a non-hibernator, from the hypothermic nadir. In particular, at the nadir, the glycogen synthase kinase-{beta} was largely inhibited in both regions, the antiapoptotic factor AKT was significantly activated in the hippocampus, and melatonin plasma levels were significantly increased, while a transient neuroinflammation was observed during the recovery period. Together, the present data suggest that ST can trigger a previously undescribed latent and regulated physiological process, that is able to cope with brain PPTau formation. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=113 SRC="FIGDIR/small/485745v3_ufig1.gif" ALT="Figure 1"> View larger version (56K): org.highwire.dtl.DTLVardef@12e4ccdorg.highwire.dtl.DTLVardef@b44201org.highwire.dtl.DTLVardef@598a7corg.highwire.dtl.DTLVardef@92df61_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2021

Neurons in the dorsomedial hypothalamus promote, prolong, and deepen torpor

Torpor is a naturally occurring, hypometabolic, hypothermic state engaged by a wide range of animals in response to imbalance between the supply and demand for nutrients. Recent work has identified some of the key neuronal populations involved in daily torpor induction in mice, in particular projections from the preoptic area of the hypothalamus (POA) to the dorsomedial hypothalamus (DMH). The DMH plays a role in thermoregulation, control of energy expenditure, and circadian rhythms, making it well positioned to contribute to the expression of torpor. We used activity dependent genetic TRAPing techniques to target DMH neurons that were active during natural torpor bouts in female mice. Chemogenetic reactivation of torpor-TRAPed DMH neurons in calorie-restricted mice promoted torpor, resulting in longer and deeper torpor bouts. Chemogenetic inhibition of torpor-TRAPed DMH neurons did not block torpor entry, suggesting a modulatory role for the DMH in the control of torpor. This work adds to the evidence that the POA and the DMH form part of a circuit within the mouse hypothalamus that controls entry into daily torpor. SignificanceDaily heterotherms such as mice employ torpor to cope with environments in which the supply of metabolic fuel is not sufficient for the maintenance of normothermia. Daily torpor involves reductions in body temperature, as well as active suppression of heart rate and metabolism. How the central nervous system controls this profound deviation from normal homeostasis is not known, but a projection from the preoptic area to the dorsomedial hypothalamus has recently been implicated. We demonstrate that the dorsomedial hypothalamus contains neurons that are active during torpor. Activity in these neurons promotes torpor entry and maintenance, but their activation alone does not appear to be sufficient for torpor entry.

neuroscience↗

bioRxiv2019

Paternally expressed imprinted Snord116 and Peg3 regulate hypothalamic orexin neurons

Imprinted genes are highly expressed in the hypothalamus; however, whether specific imprinted genes affect hypothalamic neuromodulators and their functions is unknown. It has been suggested that Prader-Willi syndrome (PWS), a neurodevelopmental disorder caused by lack of paternal expression at chromosome 15q11-q13, is characterised by hypothalamic insufficiency. Here, we investigate the role of the paternally expressed Snord116 gene within the context of sleep and metabolic abnormalities of PWS, and we report a novel role of this imprinted gene in the function and organisation of the two main neuromodulatory systems of the lateral hypothalamus (LH), namely, the orexin (OX) and melanin concentrating hormone (MCH) systems. We observe that the dynamics between neuronal discharge in the LH and the sleep-wake states of mice with paternal deletion of Snord116 (PWScrm+/p-) are compromised. This abnormal state-dependent neuronal activity is paralleled by a significant reduction in OX neurons in the LH of mutants. Therefore, we propose that an imbalance between OX- and MCH-expressing neurons in the LH of mutants reflects a series of deficits manifested in the PWS, such as dysregulation of rapid eye movement (REM) sleep, food intake and temperature control.\n\nHighlightsO_LISnord116 regulates neuronal activity in the lateral hypothalamus (LH), which is time-locked with cortical states of sleep.\nC_LIO_LILoss of Snord116 reduces orexin neurons in the LH and affects sleep homeostasis and thermoregulation in mice.\nC_LIO_LISnord116 and Peg3 independently control orexin expression in the LH.\nC_LIO_LIPaternally expressed alleles maximize the patrilineal effects in the control of REM sleep by the LH in mammals.\nC_LI

neuroscience↗

bioRxiv2019

The paternally imprinted gene Snord116 regulates cortical neuronal activity

Prader-Willi syndrome (PWS) is a neurodevelopmental disorder that is characterized by rapid eye movement (REM) sleep abnormalities. The disease is caused by genomic imprinting defects that are inherited through the paternal line. Among the genes located in the PWS region on chromosome 15 (15q11-q13), small nucleolar RNA 116 (Snord116) has been previously associated with intrusions of REM sleep into wakefulness in both humans and mice.\n\nHere, we further explore the processes of sleep regulation by studying the PWScrm+/p- mouse line, which carries a paternal deletion of Snord116. We focused on microstructural electrophysiological components of sleep, such as REM sleep features and sleep spindles within NREM sleep. While the former are thought to contribute to neuronal network formation early in brain development, the latter are markers of thalamocortical processes. Both signals are often compromised in neurodevelopmental disorders and influence functional properties of cortical neurons. Thus, we isolated and characterized the intrinsic activity of cortical neurons using in vitro microelectrode array (MEA) studies.\n\nOur results indicate that the Snord116 gene in mice selectively influences REM sleep properties, such as theta rhythms and the organization of REM episodes throughout sleep-wake cycles. Moreover, sleep spindles present specific abnormalities in PWS model systems, indicating that these features of sleep may translate as potential biomarkers in human PWS. We observed abnormalities in the synchronization of cortical neuronal activity that are accounted for by high levels of norepinephrine.\n\nIn conclusion, our results provide support for an important role of Snord116 in regulating brain activity during sleep and, in particular, cortical neuronal properties, thereby opening new avenues for developing interventions in PWS.\n\nSignificance StatementWe found that the Snord116 gene, a major player in Prader-Willi syndrome (PWS), significantly impacts REM sleep and its regulation. Additionally, we found that sleep spindles, a subtle electroencephalography (EEG) marker that occurs during NREM sleep, are dysregulated in PWS mice that carry a paternal deletion of the Snord116 gene. Using a combination of in vivo and in vitro experiments, we identified sleep features at the network and molecular level that suggest that Snord116 is fundamental in the synchronization of neuronal networks. Our study also provides a new pre-clinical tool to investigate the pathophysiology of sleep in PWS.

neuroscience↗