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Vincent, C.

Publications and source records attributed to Vincent, C..

15 recordsLinked to original sources

Phloem-Limited Disease Impacts Citrus Carbohydrate Dynamics Distinctly from Source-Sink Manipulation

Source-sink dynamics are defined by the interdependence of source and sink tissues and are key determinants of plant growth and productivity. This dynamic can, be altered by disease. One example is huanglongbing (HLB), a phloem-limited disease that impacts several economically important tree species by disrupting carbon partitioning and altering source-sink relationships. Though HLB is widespread in citrus, the specific mechanism in which phloem disruption impacts the co-regulation of carbon dynamics from source to sink has not been fully described. To address this, we took advantage of a natural study under field conditions, in which infected and uninfected trees were growing in the same field. After identifying trees that were uninfected, infected with symptoms, or infected without symptoms, we manipulated source:sink ratio by girdling branches and defoliating at 0%, 50%, and 75% of the original leaf area per fruit, while leaving a control treatment with no defoliation or girdling and used fruits as the sink of interest. We measured gas exchange, biomass, and non-structural carbohydrates in leaves, stems and fruits in response to these treatments. Our results show that leaf photosynthetic responses to HLB were primarily driven by stomatal regulation rather than biochemical limitations. HLB increased leaf dark respiration without altering the relationship between respiration and leaf soluble sugars. Among the plant organs, stem starch reserves were the most responsive to source-sink manipulation and were strongly correlated with multiple carbon pools and biomass in both fruits and leaves. Although HLB altered fruit carbon dynamics, it did not change fruit responses to source-sink manipulation. Overall, HLB affects source and sink tissues independently of the experimental source-sink manipulation. The stem serves as a transient carbon reserve and is sensitive to both HLB and source-sink manipulation. These findings raise further questions regarding total carbon fluxes and the importance of feedback inhibition of photosynthesis.

plant biology↗

PLANT WATER-CARBON RELATIONS IN HUANGLONGBING-AFFECTED CITRUS TREES AND THE IMPACT OF HLB EXPOSURE DURATION, FRUIT DEVELOPMENTAL STAGE, AND SOURCE-SINK MANIPULATION ON THESE RELATIONS

Bulk phloem flow is driven by pressure gradients generated by water drawn from the xylem, coupling source-sink transport with water status. Huanglongbing (HLB), a phloem-affecting bacterial disease of citrus, disrupts phloem transport, and causes canopy water deficit. Although improved water management can enhance HLB-affected tree health, the effects of HLB on water-driven source-sink relations are unknown. Fruits function as both carbon sink and water reservoir, but the role of fruit in regulating whole-tree water status remain poorly understood. We examined leaf-fruit water relations in HLB-affected citrus and evaluated how HLB exposure duration, fruit developmental stage, and source-sink manipulation shape these dynamics. Source-sink relations were manipulated in branches of symptomatic trees with long-term (four years) and recent (six months) HLB exposure. We girdled branches with a single fruit as the sink and defoliated at (0%, 50%, or 75%), and an ungirdled, non-defoliated branch served as control. We measured stomatal conductance, leaf hydraulic traits, leaf and fruit soluble sugars, diurnal fruit shrinkage (to estimate xylem backflow) and fruit water loss. Source-sink manipulation did not affect shoot total soluble sugar. HLB-exposure resulted in less negative osmotic potential, more negative turgor potential and reduced modulus of elasticity and relative water content at turgor loss point. HLB exposure also increased diurnal fruit shrinkage, with shrinkage responses to source-sink manipulation varying across fruit development stages. Collectively, these findings suggest that long-term HLB exposure promotes leaf acclimation to water deficits, however, high sink demand may diminish the leaf water status regulation at Stage II, when fruit sink carbon demand is highest.

plant biology↗

Combating citrus greening disease by simultaneously targeting the pathogen and callose-mediated phloem occlusion

Huanglongbing (HLB), caused by Candidatus Liberibacter asiaticus (CLas), disrupts sugar transport in citrus due to bacterial proliferation and excessive callose deposition that blocks sieve elements. Unblocking phloem may reduce symptoms, but it is unclear whether targeting CLas or suppressing callose deposition is more critical, as both contribute to phloem dysfunction. This study evaluated whether an integrated strategy targeting both CLas and callose-mediated phloem blockage could more effectively restore phloem transport, carbohydrate allocation, and productivity in HLB-affected citrus. Two complementary field experiments assessed the effects of an antibiotic, a callose inhibitor, and their combination on phloem recovery and source-sink dynamics. The first experiment focused on treatment-induced changes in carbon transport between source and sink shortly after delivery via stem infiltration, capturing immediate physiological responses. The second experiment assessed cumulative carbon allocation to determine sustained effects on assimilate transport and fruit development. Callose inhibitor treatment increased sugar transport but this immediate response did not yield lasting benefits. Antibiotic treatment enhanced carbon import into developing fruits, but these effects were not consistently supported by other physiological indicators. In contrast, the combined treatment reduced callose deposition, improved phloem conductivity and carbon allocation during high sink demand, decreased fruit abscission, and increased the total carbon accumulated in the fruits after physiological fruit drop. Collectively, these results demonstrate that impaired source-sink balance in HLB-affected citrus results from the combination of both pathogen load and host callose accumulation, supporting an integrated strategy that combines pathogen suppression with modulation of host phloem function to improve orchard productivity.

plant biology↗

Citrus photosynthesis and morphology acclimate to phloem-affecting huanglongbing disease at the leaf and shoot levels

Huanglongbing (HLB) is a phloem-affecting disease of citrus that reduces growth and has impacted global citrus production. HLB is caused by a phloem-limited bacterium (Candidatus Liberibacter asiaticus; CLas). By inhibiting phloem function, HLB stunts sink growth, including reducing production of new shoots and leaves, and induces hyperaccumulation of foliar starch. HLB induces feedback inhibition of photosynthesis by reducing foliar carbohydrate export. In this work we assessed the relationship of bacterial distribution within the foliage, foliar starch accumulation, and net CO2 assimilation (Anet). Because HLB impacts canopy morphology, we developed a chamber to measure whole-shoot Anet to test the effects of HLB at both leaf and shoot levels. Whole-shoot-level Anet saturated at high irradiance, and green stems had high photosynthetic rates compared to leaves. Starch accumulation was correlated with bacterial population, and starch was negatively correlated with Anet at the leaf level but not at the shoot level. Starch increased initially after infection, then decreased progressively with increasing length of infection. HLB infection reduced Anet at the leaf level, but increased it at the whole shoot level, in association with reduced leaf size and greater relative contribution of stems to photosynthetic surface area. Although HLB-increased photosynthetic efficiency, total carbon fixed per shoot decreased because photosynthetic surface area was reduced. We conclude that the localized effects of infection on photosynthesis are mitigated by whole shoot morphological acclimation over time. Stems contribute important proportions of whole shoot Anet, and these contributions are likely increased by the morphological acclimation induced by HLB.

plant biology↗

Dysregulated myogenesis and autophagy in genetically induced pulmonary emphysema

Patients with chronic obstructive pulmonary disease (COPD)-pulmonary emphysema often develop locomotor muscle dysfunction, which is independently associated with disability and higher mortality in that population. Muscle dysfunction entails reduced muscle mass and force-generation capacity, which are influenced by fibers integrity. Myogenesis, which is muscle turnover driven by progenitor cells such as satellite cells, contributes to the maintenance of muscle integrity in the context of organ development and injury-repair cycles. Injurious events crucially occur in COPD patients skeletal muscles in the setting of exacerbations and infections which lead to acute decompensations for limited periods of time after which, patients typically fail to recover the baseline status they had before the acute event. Autophagy, which is dysregulated in muscles from COPD patients, is a key regulator of satellite cells activation and myogenesis, yet very little research has so far investigated the mechanistic role of autophagy dysregulation in COPD muscles. Using a genetically inducible murine model of COPD-driven muscle dysfunction and confirmed with a second genetic animal model, we found a significant myogenic dysfunction associated with a reduced proliferative capacity of freshly isolated satellite cells. Transplantation experiments followed by lineage tracing suggest that an intrinsic defect in satellite cells, and not in the COPD environment, plays a dominant role in the observed myogenic dysfunction. RNA sequencing analysis of freshly isolated satellite cells suggests dysregulation of transcripts associated with control of cell cycle and autophagy, which is confirmed by a direct observation of COPD mice satellite cells fluorescent-tracked autophagosome formation. Moreover, spermidine-induced autophagy stimulation leads to improved satellite cells autophagosome turnover, replication rate and myogenesis. Our data suggests that pulmonary emphysema causes a disrupted myogenesis, which could be improved with stimulation of autophagy and satellite cells activation, leading to an attenuated muscle dysfunction in this context.

physiology↗

Phloem transport limitation in Huanglongbing affected sweet orange is dependent on phloem-limited bacteria and callose

Huanglongbing (HLB), caused by Candidatus Liberibacter asiaticus (CLas), is a phloem-limited disease which disrupts citrus production in affected areas. In HLB-affected plants, phloem sieve plate pores accumulate callose, and leaf carbohydrate export is reduced. However, whether HLB causes a reduction in carbohydrate phloem translocation speed, and the quantitative relationships among callose, CLas population, and phloem translocation are still unknown. In this work, a procedure was developed to concurrently measure sugar transport, callose deposition, and relative pathogen population at different locations throughout the stem. Increasing quantities of CLas genetic material were positively correlated with quantity and density of callose deposits, and negatively correlated with phloem translocation speed. Callose deposit quantity was site- and rootstock dependent, and were negatively correlated with phloem translocation speed, suggesting a localized relationship. Remarkably, callose accumulation and phloem translocation disruption in the scion was dependent on rootstock genotype. Regression results suggested that the interaction of Ct values and number of phloem callose depositions, but not their size or density, explained the effects on translocation speed. Sucrose, starch, and sink 14C label allocation data support the interpretation of a transport pathway limitation by CLas infection. This work shows that the interaction of local accumulation of callose and CLas affect phloem transport. Further, the extent of this accumulation is attenuated by the rootstock and provides important information about the disease mechanism of phloem-inhabiting bacteria. Together, these results constitute the first example of a demonstrated transport limitation of phloem function by a microbial infection.

plant biology↗

Knocking out AtCALS7 disturbs photoassimilate distribution and weakens defence against phytoplasma infection

Callose deposition around sieve pores, under control of callose synthase 7 (AtCALS7), has been interpreted as a mechanical response to limit pathogen spread in phytoplasma-infected plants. Wild-type and Atcals7ko mutants were therefore employed to unveil the mode of involvement of CALS7 in the plants response to phytoplasma infection. The fresh weights of healthy and CY-(Chrysanthemum Yellows) phytoplasma-infected Arabidopsis wild-type and mutant plants indicated two superimposed effects of the absence of CALS7: a partial impairment of photo-assimilate transport and a stimulated phytoplasma proliferation as illustrated by a significantly increased phytoplasma titre in Atcal7ko mutants. Further studies solely dealt with the effects of CALS7 absence on phytoplasma growth. Phytoplasma infection affected sieve-element substructure to a larger extent in mutants than in wild-type plants, which was also true for the levels of some free carbohydrates. Moreover, infection induced a similar upregulation of gene expression of enzymes involved in sucrose cleavage (AtSUS5, AtSUS6) and transmembrane transport (AtSWEET11) in mutants and wild-type plants, but an increased gene expression of carbohydrate transmembrane transporters (AtSWEET12, AtSTP13, AtSUC3) in infected mutants only. It remains still unclear how the absence of AtCALS7 leads to gene upregulation and how an increased intercellular mobility of carbohydrates and possibly effectors contributes to a higher susceptibility. It is also unclear if modified sieve-pore structures in mutants allow a better spread of phytoplasmas giving rise to higher titre. Author SummaryPhytoplasma infections are one of the most limiting factors for production of important crops all over the world. Phytoplasma disease epidemics can be handled mainly by insect-vector control using insecticides. Basic information about plant-phytoplasma interactions are still limited, nevertheless it is necessary to design new management and breeding strategies aimed to obtain more tolerant or resistant cultivars. Phytoplasmas are obligate intracellular parasites restricted to the phloem sieve tubes. Callose deposition at the sieve plates has been described since the 70s as a mechanical defence process to limit pathogen spread by occluding sieve pores. Studies reported 40 years later demonstrated that callose at the sieve pores is also involved in sieve-pore development and function and, hence, in mass-flow regulation, carbohydrate metabolism and distribution, and plant growth. Here, we reported on the role(s) of sieve-element callose in phytoplasma-infected Arabidopsis, using a mutant lacking AtCALS7, the enzyme responsible for callose synthesis in the sieve elements. The results indicate that loss of AtCAL7 appears to confer increased susceptibility to phytoplasma infection, due to alterations in expression of genes involved in sugar metabolism and membrane transport. In the long run, the identification of plant resistance or susceptibility traits against phytoplasmas will allow a complete re-organization of chemical control strategies, with obvious opportunities of reducing insecticide burden.

plant biology↗

Succinate Dehydrogenase (SDH)-subunit C regulates muscle oxygen consumption and fatigability in an animal model of pulmonary emphysema.

Patients with pulmonary emphysema often develop locomotor muscle dysfunction, which is independently associated with disability and higher mortality in that population. Muscle dysfunction entails reduced force-generation capacity which partially depends on fibers oxidative potential, yet very little mechanistic research has focused on muscle respiration in pulmonary emphysema. Using a recently established animal model of pulmonary emphysema-driven skeletal muscle dysfunction, we found downregulation of succinate dehydrogenase (SDH) subunit C in association with lower oxygen consumption and fatigue-tolerance in locomotor muscles. Reduced SDH activity has been previously observed in muscles from patients with pulmonary emphysema and we found that SDHC is required to support respiration in cultured muscle cells. Moreover, in-vivo gain of SDH function in emphysema animals muscles resulted in better oxygen consumption rate (OCR) and fatigue tolerance. These changes correlated with a larger number of relatively more oxidative type 2-A and 2X fibers, and a reduced amount of 2B fibers. Our data suggests that SDHC is a key regulator of respiration and fatigability in pulmonary emphysema-driven skeletal muscles, which could be impactful to develop strategies aimed at attenuating this comorbidity.

physiology↗

In vitro assessment of the virucidal activity of four mouthwashes containing Cetylpyridinium Chloride, ethanol, zinc and a mix of enzyme and proteins against a human coronavirus

Backgroundsaliva is established to contain high counts SARS-CoV-2 virus and contact with saliva droplets, contaminated surfaces or airborne particles are sources of viral transmission. The generation of infective aerosols during clinical procedures is of particular concern. Therefore, a fuller understanding of the potential of mouthwash to reduce viral counts and modulate the risk of transmission in medical professional and public context is an important research topic. Methodwe determined the virucidal activity of four anti-bacterial mouthwashes against a surrogate for SARS-CoV-2, Human CoV-SARS 229E, using a standard ASTM suspension test, with dilution and contact times applicable to recommended mouthwash use. Resultsthe mouthwash formulated with 0.07% Cetylpyridinium Chloride exhibited virucidal effects providing a [≥]3.0 log reduction HCoV-229E viral count. Mouthwashes containing 15.7% ethanol, 0.2% zinc sulphate heptahydrate and a mix of enzymes and proteins did not demonstrate substantive virucidal activity in this test. Conclusionmouthwash containing 0.07% Cetylpyridinium Chloride warrants further laboratory and clinical assessment to determine their potential benefit in reducing the risk of SARS-CoV-2. HighlightsSARS-CoV-2 can be transmitted through contact with infective saliva. Studies are needed to understand if mouthwash can lower SARS-CoV-2 transmission risk. 0.07% Cetylpyridinium Chloride (CPC) mouthwash exhibited virucidal effects against HCoV-SARS 229E. Further studies on potential of 0.07% CPC mouthwash against SARS-CoV-2 are warranted.

microbiology↗

Racing against stomatal attenuation: rapid CO2 response curves more reliably estimate photosynthetic capacity than steady state curves in a low conductance species

A/Ci curves are an important gas-exchange-based approach to understanding the regulation of photosynthesis, describing the response of net CO2 assimilation (A) to leaf internal concentration of CO2 (Ci). Low stomatal conductance species pose a challenge to the measurement of A/Ci curves by reducing the signal-to-noise ratio of gas exchange measures. Additionally, the stomatal attenuation effect of elevated ambient CO2 leads to further reduction of conductance and may lead to erroneous interpretation of high Ci responses of A. Rapid A/Ci response (RACiR) curves offer a potential practice to develop A/Ci curves faster than the stomatal closure response to elevated CO2. We used the moderately low conductance Citrus to compare traditional steady state (SS) A/Ci curves with RACiR curves. SS curves failed more often than RACiR curves. Overall parameter estimates were the same between SS and RACiR curves. When low stomatal conductance values were removed, triose-phosphate utilization (TPU) limitation estimates increased. Overall RACiR stomatal conductance values began and remained higher than SS values. Based on the comparable resulting parameter estimates, higher likelihood of success and reduced measurement time, we propose RACiR as a valuable tool to measure A/Ci responses in low conductance species.

plant biology↗

Form, function, and divergence of a generic fin shape in small cetaceans

Tail flukes as well as the dorsal fin are the apomorphic traits of cetaceans appeared during evolutionary process of adaptation to the aquatic life. Both appendages present a generic wing-like shape associated with lift generation and low drag. Variability of the form of appendages was studied in seven species of cetaceans having different body size, external morphology, and specialization. Hydrodynamic performance of the fin cross-sections was examined with the CFD software and compared with similar engineered airfoils. Affinity of hydrodynamic design of both appendages was found in a wing-like planform and cross-sectional design optimized for lift generation. Distinctions in the planform and cross-sections were found related with the fin specialization in thrust production or swimming stability control. Cross-sectional design of the dorsal fin was found to be optimized for the narrow range of small angles of attack. Cross-sections of tail flukes were found to be more stable for higher angles of attack and had gradual stall characteristics that is associated with their propulsive efficiency as oscillating foils. The results obtained are the evidence of divergent evolutionary pathways of a generic wing-like shape of the fins of cetaceans under specific demands of thrust production and swimming stability control.

evolutionary biology↗

OTX2 non-cell autonomous activity regulates inner retinal function

OTX2 is a homeoprotein transcription factor expressed in photoreceptors and bipolar cells in the retina. OTX2, like many other homeoproteins, transfers between cells and exerts non-cell autonomous effects such as promoting survival of retinal ganglion cells that do not express the protein. Here we used a genetic approach to target extracellular OTX2 in the retina by conditional expression of a secreted single chain anti-OTX2 antibody. Compared to control mice, the expression of this antibody by Parvalbumin-expressing neurons in the retina is followed by a reduction in visual acuity in one-month-old mice with no alteration of the retinal structure or cell type number or aspect. A- and b-waves measured by electroretinogram were also indistinguishable from control mice, suggesting no functional deficit of photoreceptors and bipolar cells. Mice expressing the OTX2-neutralizing antibody did show a significant doubling in the flicker amplitude, consistent with a change in inner retinal function. Our results show that interfering in vivo with OTX2 non-cell autonomous activity in the postnatal retina leads to an alteration in inner retinal cell functions and causes a deficit in visual acuity. Significance statementOTX2 is a homeoprotein transcription factor expressed in retinal photoreceptors and bipolar cells. Although the Otx2 locus is silent in the inner retina, the protein is detected in cells of the ganglion cell layer consistent with the ability of this class of proteins to transfer between cells. We expressed a secreted single chain antibody (scFv) against OTX2 in the retina to neutralize extracellular OTX2. Antibody expression leads to reduced visual acuity with no change in retinal structure, or photoreceptor or bipolar physiology; however, activity in the inner retina was altered. Thus, interfering with OTX2 non-cell autonomous activity in postnatal retina alters inner retinal function and causes vision loss, highlighting the physiological value of homeoprotein direct non-cell autonomous signaling.

neuroscience↗

The latitudinal gradient in hand-wing-index: global patterns and predictors of wing morphology in birds

An organisms ability to disperse influences many fundamental processes in ecology. However, standardised estimates of dispersal ability are rarely available, and thus the patterns and drivers of broad-scale variation in dispersal ability remain unclear. Here we present a global dataset of avian hand-wing index (HWI), an estimate of wingtip pointedness widely adopted as a proxy for flight efficiency and dispersal in birds. We show that HWI is correlated with geography and ecology across 10,391 (>99 %) bird species, increasing at higher latitudes and in migratory and/or non-territorial species. After controlling for these effects, the strongest predictor of HWI is temperature variability (i.e. seasonality), with secondary effects of diet and habitat type. Our analyses (1) reveal a prominent latitudinal gradient in HWI shaped by ecological and environmental factors, and (2) provide a global index of avian dispersal ability for wider use in community ecology, macroecology, and macroevolution.\n\nStatement of authorshipThe study was conceived by CS and JAT. Data collection was led by JAT, SC, and CS, with contributions from CS, MNC, NA, SEIJ, CV, HEAM, TPB, and SC. CS performed the analyses. CS and JAT wrote the manuscript and all authors revised the text.

evolutionary biology↗

Non-cell autonomous OTX2 transcription factor regulates anxiety-related behaviors in the mouse

The Otx2 homeoprotein transcription factor is expressed in the dopaminergic neurons of the ventral tegmental area, a mesencephalic nucleus involved in the control of complex behaviors through its projections to limbic structures, including the ventral hippocampus, amygdala, nucleus accumbens and medial prefrontal cortex. We find adult mice heterozygous for Otx2 show anxiolysis-like phenotype in light-dark box and elevated plus maze paradigms. However, the number of dopaminergic neurons, the integrity of their axons, their projection patterns in target structures, and the amounts of dopamine and dopamine metabolites in targets structures were not modified. Because OTX2 is expressed by the choroid plexus, secreted into cerebrospinal fluid and transferred to parvalbumin interneurons of the cortex, hippocampus, and amygdala, we investigated if this phenotype could result from the decreased synthesis of OTX2 in the choroid plexus. Indeed, the anxiolysis-like phenotype was partially recapitulated in the Otx2+/AA and scFvOtx2tg/0 choroid-plexus dependent non-cell-autonomous OTX2 loss of function mouse models. Furthermore, the phenotype was reversed by the overexpression of Otx2 specifically in choroid plexus of adult Otx2 heterozygous mice. Taken together, OTX2 synthesis by the choroid plexus followed by its secretion into the cerebrospinal fluid is an important regulator of the anxiety phenotype in the mouse.

neuroscience↗

Ki-67 supports global gene expression programmes driving tumourigenesis

Recent studies have shown that the cell proliferation antigen Ki-67 is not required for cell proliferation. Here, we demonstrate that Ki-67 enables implementation of transcriptional programmes conferring cellular plasticity, and is required for each step of tumour initiation, growth and metastasis. Ki-67 knockout causes global transcriptome remodelling, which, in mammary carcinoma cells, inhibits the epithelial-mesenchymal transition in a polycomb-repressive complex 2-dependent manner. This results in suppression of stem cell characteristics and sensitisation to various drug classes. Cancer cells lacking Ki-67 proliferate normally in vivo, but tumour growth is inhibited due to disrupted angiogenesis, and metastasis is abrogated. Finally, mice lacking Ki-67 are resistant to chemical or genetic induction of intestinal tumourigenesis. Thus, Ki-67, which is expressed in all proliferating cancer cells, confers the plasticity required for different steps of carcinogenesis.

cancer biology↗