Biology subjects

Rossi, L.

Publications and source records attributed to Rossi, L..

At least 19 recordsLinked to original sources

bioRxiv2026

NAD+ limitation and α-ketoglutarate depletion define cancer induced muscle atrophy

Tumour-host crosstalk is an emerging hallmark of malignancy. It is increasingly recognised that cancer alters non-tumour bearing distant organs, with important consequences for disease progression and survival. Skeletal muscle loss, a defining feature of cancer-associated cachexia, contributes to morbidity and reduced quality of life, yet its underlying mechanisms remain poorly understood. In this study we analysed the secretome of pancreatic cancer cells and identified a metabolite-driven signal that induces myotube atrophy. Our data suggests that atrophy, which seems to involve cytoskeletal stress and increased myosin contractility, arises from cancer cell-dependent reductive metabolic rewiring. Pancreatic cancer cells conditioned their environment with elevated levels of lactate, generating a lactate-rich extracellular milieu that decrease the NAD+/NADH ratio in myotubes. This redox imbalance impaired oxidative metabolism, decreasing -ketoglutarate (KG) levels and disrupted KG-dependent processes. Restoration of NAD+ or KG levels rescued myotube atrophy. Skeletal muscle from cancer-associated cachexia mouse models exhibited reduced KG levels. Collectively, these findings identify a targetable metabolite-mediated mechanism of tumour-muscle crosstalk.

cancer biology↗

bioRxiv2026

Integrated metabolic and proteostatic profiling reveals remodeling of proteolytic pathways associated with redox-bioenergetic dysfunction in a PAHenu2 mouse model of phenylketonuria

Phenylketonuria (PKU) is a genetic metabolic disorder caused by the lack of functional phenylalanine hydroxylase (PAH). Elevated levels of phenylalanine (Phe) are known to be neurotoxic; however, the molecular mechanisms underlying Phes effects remain elusive. This study investigates the impact of PKU on proteostasis, redox balance, and metabolism in BTBR PAHenu2 mice, a severe disease animal model. Combined proteomics and metabolomics revealed impaired redox homeostasis in the brain and disrupted mitochondrial energy metabolism (ATP and TCA intermediates). The dysregulation was further supported by decreased levels of ATP, reduced glutathione (GSH), cysteine, and reduced catalase activity. Western blot analyses revealed substantial remodeling of protein degradation systems: the 19S regulatory (Rpt1) subunit and 26S proteasome content and activity were significantly increased, and ubiquitinated protein levels were elevated, indicating protein turnover and activation of the ubiquitin-proteasome system. Autophagy was also activated, as evidenced by a reduced LC3-II/LC3-I ratio, decreased p62 levels, unchanged ATG5 levels, and increased HSPA8 protein expression. By contrast, UPR markers remained stable despite an increase in the oxidized-to-reduced PDI ratio, suggesting a localized shift without activation of a full ER stress response. In parallel, systemic alterations were assessed in whole blood. Indeed, GSH, cysteine, ATP and ADP were decreased in PKU, whereas NADPH increased. These changes were accompanied by reduced activities of GSH reductase and GSH peroxidase, thereby confirming metabolic and redox disruption. Collectively, these findings indicate that PKU is associated with activation of protein degradation pathways as an adaptive response to cellular stress combined with redox imbalance and energy dysregulation. Highlights- Proteasome complex levels and activity were upregulated in PAHenu2 mouse brains - Autophagy was also enhanced in PAHenu2 mouse brains - Despite increased PDI oxidation, the Unfolded Protein Response was not activated - Redox and energy metabolism were disrupted in both brain and blood

molecular biology↗

bioRxiv2026

Vegetation increases CH4 emissions and methanotroph diversity in marine sediments

Seagrass meadows are key blue carbon (C) ecosystems, storing large amounts of organic C over centuries. Their climate benefits may be reduced by methane (CH) emissions, whose microbial and environmental descriptors in Zostera noltei meadows, dominant seagrass in North-Western Europe, remain poorly understood. We studied CH fluxes, CH-producing and consuming microbial communities and sediment physico-chemical parameters in Z. noltei meadows and adjacent bare sediments across seven sites in Arcachon Bay, France. In situ CH fluxes were measured at low tide and microbial communities were characterised using targeted metagenomics of three functional genes (mcrA, mmoX, pmoA) and quantitative PCR. CH fluxes were higher in vegetated than bare sediments (24.4 {+/-} 2.6 vs. 9.4 {+/-} 0.7 {micro}mol m-{superscript 2} d-{superscript 1}). Mixed linear models and random forest analyses identified C accumulation rate and CO2 flux as the strongest positive descriptors of CH fluxes. Vegetated sediments hosted more diverse methanotrophs, while methanogens showed no habitat differences. Four genera (mcrA-Methanolobus, mmoX-Methylocella, pmoA-Methylococcus, Methyloglobulus) emerged as abundant, seagrass-associated, correlated with CH fluxes, and highlighted by models. Functional diversity, especially pmoA richness, was a stronger microbial descriptor of CH fluxes than gene abundance or a specific genus. Findings indicate Z. noltei meadows enhance C burial and CH emission, with methanotroph diversity potentially mitigating CH emissions. Our results provide the first integrated assessment of CH fluxes and their descriptors in Z. noltei meadows, highlighting the intertwined nature of C burial and CH emissions and the need to account for both in blue C climate assessments.

ecology↗

bioRxiv2025

Advanced human iPSC-based modelling of LMNA-related congenital muscular dystrophy enables development of targeted genetic therapies for muscle laminopathies

LMNA-related congenital muscular dystrophy (L-CMD) is amongst the most severe forms of laminopathies, which are diseases caused by pathogenic variants in the LMNA gene. LMNA encodes the proteins Lamin A and C, which assemble with Lamin B1 and B2 to form the nuclear lamina: a meshwork providing structural stability to the nucleus that also regulates chromatin organisation and gene expression. Research into L-CMD mechanisms and therapies is hindered by lack of humanised, tissue-specific models that accurately recapitulate disease phenotypes. We previously reported that LMNA-mutant induced pluripotent stem cell (iPSC)-derived skeletal muscle cells have nuclear shape abnormalities and Lamin A/C protein mislocalisation. Here, we expand the selection of L-CMD patient- derived iPSCs and validate disease-associated readouts using a transgene-free based protocol which more accurately mimics skeletal myogenesis. Results showed no overt defects in developmental myogenesis, but recapitulation of pathological nuclear shape abnormalities in 2D and 3D cultures, nuclear envelope protein mislocalisation and transcriptomic alterations across multiple pathogenic LMNA variants. We then utilised this platform to assess LMNA gene editing strategies. CRISPR-based exon removal generated stable RNA and protein Lamin A/C species, without significant normalisation of nuclear morphological phenotypes or transcriptomic profile. Conversely, precise editing of the same mutation showed complete reversal of disease-associated nuclear morphometrics, alongside normalisation of the pro-inflammatory transcriptomic signature. Our data provide the foundation for a humanised in vitro disease and therapy modelling platform for this complex and severe muscle disorder. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=81 SRC="FIGDIR/small/660928v2_ufig1.gif" ALT="Figure 1"> View larger version (15K): org.highwire.dtl.DTLVardef@134276forg.highwire.dtl.DTLVardef@108f44forg.highwire.dtl.DTLVardef@dfa04eorg.highwire.dtl.DTLVardef@1956a90_HPS_FORMAT_FIGEXP M_FIG C_FIG HIGHLIGHTSO_LILMNA-mutant iPSCs undergo efficient skeletal myogenesis upon transgene-free, small molecule-based lineage-directed differentiation C_LIO_LIL-CMD iPSCs recapitulate hallmark disease-associated nuclear phenotypes and show a pro-inflammatory transcriptional profile C_LIO_LIDisease modelling platforms based on iPSC-derived skeletal muscle cells enable comparative testing of gene editing strategies C_LIO_LICRISPR-edited L-CMD iPSC-derived myogenic cells show amelioration of disease-associated readouts C_LI

cell biology↗

bioRxiv2025

The "Grove-First" Framework: Starting in the Grove to Find Therapies for Huanglongbing

Citrus greening disease, also known as huanglongbing (HLB), is the most serious vector-borne bacterial disease of citrus world-wide1,2. There is an immediate global need to provide the citrus industry with relief from HLB and a return to profitable citrus production. Standard screening methods for HLB therapeutic treatments typically involve various laboratory-based assays to select treatments with antimicrobial properties3, which then advance to greenhouse and eventually field testing in a workflow that takes multiple years. Unlike traditional lab-first screening, we present a design of experiments framework4,5, referred to as Grove-First, that rapidly screens treatments with regulatory-friendly profiles in commercial citrus groves using trunk injection to select treatments that improve tree health and fruit yield over the course of a single growing season. Using this framework, we identified candidate treatments with effects comparable to or better than the standard oxytetracycline (OTC) on visual tree-health and/or yield indices in an initial screen of HLB-positive 8-year-old Valencia sweet orange trees. Expanded trials in commercial citrus groves allowed us to validate the initial screening results at other locations and in other citrus varieties. Grove-First rapidly accelerated the identification and large-scale field testing of HLB therapies, some of which are available for growers to use immediately and others that require further field testing and/or regulatory actions.

plant biology↗

bioRxiv2024

Engineering assembloids to mimic graft-host skeletal muscle interaction

Skeletal muscle (SkM) tissue engineering aims to generate in vitro three-dimensional (3D) products that can be implanted in patients to replace or repair damaged muscles. Having a humanized in vitro model able to mimic the interaction between the innervated recipient and the engineered SkMs at a functional level would greatly help in the evaluation of the graft potential. Here we developed a 3D in vitro model that allowed to investigate the function, stability, and adaptability of the human NM system in response to an engineered SkM construct. To achieved this, we used decellularized SkMs (dSkM)-based constructs as engineered SkM and human neuromuscular organoids (NMOs) as the recipient-like NM system to create graft-host SkM assembloids. We observed migration of myogenic cells and invasion of neural axons from the NMO to the engineered SkM construct in the assembloids, with the generation of functional neuromuscular junctions (NMJs). Finally, we showed that assembloids were able to regenerate following acute damage, with SkM regeneration and functional recovery. Despite limited by the absence of immunocompetent cells and vasculature, our data showed that our assembloid represents a useful tool to evaluate in vitro the response of the human innervated SkM to a potential tissue-engineered SkM graft.

cell biology↗

bioRxiv2024

Detecting microbial engraftment after FMT: sorting signals from noise using placebo sequencing and culture-enriched metagenomics

Fecal microbiota transplantation (FMT) has shown efficacy for the treatment of ulcerative colitis but with variable response between patients and trials. The mechanisms underlying FMTs therapeutic effects remains poorly understood but is generally assumed to involve engraftment of donor microbiota into the recipients microbiome. Previous studies have reported microbial engraftment following FMT in various disease contexts but with inconsistent results between studies. Here we investigate engraftment in UC patients receiving FMT from a single donor applying amplicon-based profiling, shotgun metagenomics and culture-enriched metagenomics. Placebo samples were included to estimate engraftment noise, and a significant level of false-positive engraftment was observed which confounds the prediction of true engraftment. We show that analyzing engraftment across multiple patients from a single donor enhances the accuracy of detection. We identified a unique set of genes engrafted in responders to FMT which supports strain displacement as the primary mechanism of engraftment in our cohort.

microbiology↗

bioRxiv2024

Diversity and assembly of the microbiome of a leguminous plant along an urbanization gradient

Interactions between plants and bacterial communities are essential for host physiology and broader ecosystem functioning, but plant-microbiome interactions can be disrupted by environmental change like urbanization. Here, we evaluated how urbanization affected the diversity and assembly of soil and white clover (Trifolium repens) microbiome communities. We sampled 35 populations of white clover and associated roots and soil along an urbanization gradient. Soil alpha diversity was greater at the urban and rural limits of the gradient and lower in suburban habitats, while root alpha diversity was not influenced by urbanization. Root and soil bacterial communities had distinct compositions, with greater beta diversity for root compared to soil microbiomes. We found that urbanization directly and indirectly affected soil microbiome assembly, particularly through soil carbon. In contrast, root microbiome assembly was not linked to urbanization, which suggested that the host plant acted as an additional filter on microbiome assembly independent of urbanization. We also found that key pathogenic bacteria like Legionella and Clostridium varied in abundance with urbanization, which has implications for human health. Together, our study underscores the importance of examining how urban-driven environmental change alters the ecology and function of soil and root microbiomes.

ecology↗

bioRxiv2024

Engineered Oxalate decarboxylase boosts activity and stability for biological applications

Oxalate decarboxylase (OxDC) from Bacillus subtilis is a Mn-dependent hexameric enzyme which converts oxalate to carbon dioxide and formate. Recently, OxDC has attracted the interest of the scientific community, due to its biotechnological and medical applications for the treatment of hyperoxalurias, a group of pathologic conditions associated with excessive oxalate urinary excretion due to either increased endogenous production or increased exogenous absorption. The fact that OxDC displays optimum pH in the acidic range, represents a big limitation for most biotechnological applications involving processes occurring at neutral pH, where the activity and stability of the enzyme are remarkably reduced. Here, through bioinformatics-guided protein engineering, followed by combinatorial mutagenesis and analyses of activity and thermodynamic stability, we identified a double mutant of OxDC endowed with enhanced catalytic efficiency and stability under physiological conditions. The obtained engineered form of OxDC offers a potential tool for improved intestinal oxalate degradation in hyperoxaluria patients.

biochemistry↗

bioRxiv2024

Structure of hepatitis B/D antiviral drug Bulevirtide bound to its receptor protein NTCP

Cellular entry of the hepatitis B and D viruses (HBV/HDV) require binding of the viral surface polypeptide preS1 to the hepatobiliary transporter NTCP. This interaction can be blocked by bulevirtide (BLV, formerly Myrcludex B), a preS1 derivative and approved drug for treating HDV infection. To elucidate the basis of this inhibitory function, we determined a cryo-EM structure of BLV-bound human NTCP. BLV forms two domains, a plug lodged in the bile salt transport tunnel of NTCP and a string that covers the receptors extracellular surface. The N-terminally attached myristoyl group of BLV interacts with the lipid-exposed surface of NTCP. Our structure reveals how BLV inhibits bile salt transport, rationalizes NTCP mutations that decrease the risk of HBV/HDV infection, and provides a basis for understanding the host specificity of HBV/HDV. Our results provide opportunities for structure-guided development of inhibitors that target HBV/HDV docking to NTCP.

biochemistry↗

bioRxiv2023

Genetic evidence of a hybrid swarm between Alpine ibex and domestic goat

Improving the understanding of the causes and effects of anthropogenic hybridization is fundamental to ensure the conservation of wild species, particularly in the case of hybridization between wild species and their domestic relatives. Knowledge is missing for many species also because of a lack of appropriate tools for hybrid identification. Here, coupling genotype and phenotype analysis, we carried out an extensive investigation of ongoing hybridization in Alpine ibex Capra ibex, a mountain ungulate of conservation concern from a genetic perspective. By genotyping at 63 diagnostic and 465 neutral SNPs 20 suspected hybrids and 126 Alpine ibex without suspicious phenotype, representing eight populations across a major part of the species distribution, we found evidence for ongoing hybridization between Alpine ibex and domestic goat. We identified different levels of hybridization including back crosses into both Alpine ibex and domestic goat. Our results suggest a lack of reproductive barriers between the two species and good survival and reproductive success of the hybrids. Hybridization was locally intense, alike a hybrid swarm, but not spread across the rest of the species distribution. Most of the hybrids were discovered in two locations in the North-West of Italy, while random sampling of individuals from different areas did not provide evidence of recent hybridization. Our method, based on Amplicon sequencing of 63 diagnostic SNPs specifically developed for this purpose, allowed us to identify hybrids and back crosses up to the 4th-5th generation and was suitable for genetic samples of different quality, although with varying levels of certainty regarding the exact number of generations passed since hybridization. Based on the paired analysis of genotype and phenotype we provide guidelines for a first identification of hybrids in the field and suggest a procedure for the reliable identification of hybrids.

evolutionary biology↗

bioRxiv2023

Native extracellular matrix promotes human neuromuscular organoid morphogenesis and function.

Human neuromuscular organoids (NMOs) derived from induced pluripotent stem cells (hiPSCs) hold a great potential to study (dys)functional human skeletal muscle (SkM) in vitro. The three-dimensional (3D) self-assembly of NMOs leads to the generation of spheroids, whose 3D organization cannot be controlled. Indeed, proper development, maturation and function of the innervated SkM require a well-defined multiscale 3D organization of the cells in a tissue-specific extracellular matrix (ECM) context. We hypothesized that extracellular structural imprinting along with hiPSC small-molecule-based differentiation could provide self-assembly guidance driving NMO morphogenesis and promoting the maturation and function of the human neuronal-coupled SkM in vitro models. We found that SkM ECM, provided as decellularized skeletal muscle, is able to reproducibly guide the morphogenesis of differentiating hiPSC toward multiscale structured tissue-like NMOs (t-NMOs). T-NMOs show contractile activity and possess functional neuromuscular junctions (NMJs), with mature neuromuscular system upon 30 days of hiPSC differentiation. We found that t-NMO could mimic altered muscle contraction upon administration of neurotoxins that act at NMJ level. Finally, we used hiPSCs derived from patients affected by Duchenne Muscular Dystrophy (DMD) to produce DMD t-NMOs that, upon neuronal stimulation, were able to mimic the altered SkM contractility and calcium dynamics typical of the disease. Altogether, our data confirm the ability of t-NMO platform to model in vitro human neuromuscular system (patho)physiology.

cell biology↗

bioRxiv2022

Genomes of the extinct Sicilian wolf reveal a complex history of isolation and admixture with ancient dogs

The Sicilian wolf represented the only population of wolves living on a Mediterranean island until the first half of the twentieth century (1930s-1960s) 1-7. Previous studies hypothesised that they remained isolated from mainland wolves from the end of the Last Glacial Maximum (LGM) 8,9, until human persecutions led them to extinction 1-7. There are only seven known Sicilian wolf specimens from the 19th and 20th century preserved in museums in Italy and recent morphometric analyses assigned them to the new subspecies Canis lupus cristaldii 10. To better understand the origins of the Sicilian wolf, and its relationship to other wolf populations, we sequenced four whole genomes (3.8x-11.6x) and five mitogenomes. We investigated the relationship between Sicilian wolves and other modern breeds to identify potential admixture. Furthermore, considering that the last land-bridge between Sicily and Italy disappeared after the LGM 11, around 17 kya, we explored the possibility that the Sicilian wolf retained ancestry from ancient wolf and dog lineages. Additionally, we explored whether the long-term isolation might have affected the genomic diversity, inbreeding levels and genetic load of the Sicilian wolf. Our findings show that the Sicilian wolves shared most ancestry with the modern Italian wolf population but are better modelled as admixed with European dog breeds, and shared traces of Eneolithic and Bronze age European dogs. We also find signatures of severe inbreeding and low genomic diversity at population and individual levels due to long-term isolation and drift, suggesting also low effective population size.

genomics↗

bioRxiv2022

High-fructose feeding suppresses cold-stimulated brown adipose tissue glucose uptake in young men independently of changes in thermogenesis and the gut microbiome

Diets rich in added sugars, especially high in fructose, are associated with metabolic diseases such as insulin resistance, and non-alcoholic fatty liver disease. Studies have shown a link between these pathologies and changes in the microbiome and its metabolites. Given the reported associations in animal models between the microbiome and brown or beige adipose tissue (BAT) function, and the alterations in the microbiome induced by high glucose or high fructose diets, we investigated the potential causal link between high glucose or fructose diets and BAT dysfunction in humans. We show that BAT glucose uptake, but not thermogenesis, is impaired by a high fructose but not high glucose diet, in the absence of changes in body mass, the gastrointestinal microbiome, and faecal short-chain fatty acids. We conclude that BAT metabolic dysfunction occurs independently from changes in gut microbiome composition, and earlier than other pathophysiological abnormalities associated with insulin resistance and dyslipidemia during fructose overconsumption in humans.

physiology↗

bioRxiv2021

Acidity and sulfur oxidation intermediate concentrations controlled by O2-driven partitioning of sulfur oxidizing bacteria in a mine tailings impoundment

Acidification of freshwater in mining impacted areas is a major global environmental problem catalyzed by sulfur-oxidizing bacteria (SOB). To date, little is known about the active bacteria in mine tailings impoundments and their environmental niches. Here, biological sulfur oxidation was investigated over four years in a mine tailings impoundment, integrating sulfur geochemistry, genome-resolved metagenomics and metatranscriptomics. We demonstrated oxygen driven niche partitioning of SOB and their metabolic pathways that explain acidity generation and thiosulfate persistence. Four chemolithoautotrophic SOB, Halothiobacillus, Thiobacillus, Sulfuricurvum and Sediminibacterium comprised 37% to 73% of the analyzed communities. The impoundment waters alternated between the dominance of Halothiobacillus versus a Thiobacillus, Halothiobacillus, Sulfuricurvum and Sediminibacterium consortia. Halothiobacillus dominance was associated with lower pH values ([~]4.3), higher [H+]/[SO42-] and lower [S2O32-], collectively indicative of extensive sulfur oxidation. Halothiobacillus, which couple sulfur oxidation via the Sox pathway to aerobic respiration or NO2- reduction, were present throughout the depth profile, yet their expression of sox genes occurred only in upper highly oxygenated waters. Conversely, when consortia of Thiobacillus, Halothiobacillus, Sulfuricurvum and Sediminibacterium dominated, recycling/disproportionating reactions were more prevalent. Thiobacillus, which dominated deeper micro-oxic/anoxic waters, oxidized sulfur primarily through the rDSR pathway, coupled to NO3-/NO2- reduction, resulting in lower [H+]/[SO42-] and higher [S2O32-] relative to upper waters. These field results mirror the Sox/rDSR-geochemical patterns of experimental SOB enrichments and reveal opportunities for biological treatments of recalcitrant reduced sulfur compounds, as well as gene-based monitoring and in situ RNA detection to predict the onset of problematic geochemistry.

microbiology↗

bioRxiv2021

Fetal gut colonization: meconium does not have a detectable microbiota before birth

Microbial colonization of the human intestine impacts host metabolism and immunity, however when colonization occurs is unclear. Although numerous studies have reported bacterial DNA in first-pass meconium samples, these samples are collected hours to days after birth. We investigated whether bacteria could be detected in meconium prior to birth. Fetal meconium (n = 20) was collected by rectal swab during elective breech Cesarean sections without labour prior to antibiotics and compared to technical and procedural controls (n = 5), first-pass meconium (neonatal meconium; n = 14), and infant stool (n = 25). Unlike first-pass meconium, no microbial signal distinct from negative controls was detected in fetal meconium by 16S rRNA gene sequencing. Additionally, positive aerobic (n = 10 of 20) and anaerobic (n = 12 of 20) clinical cultures of fetal meconium (13 of 20 samples positive in at least one culture) were identified as likely skin contaminants, most frequently Staphylococcus epidermidis, and not detected by sequencing in most samples (same genera detected by culture and sequencing in 2 of 13 samples with positive culture). We conclude that fetal gut colonization does not occur before birth, and that microbial profiles of neonatal meconium reflect populations acquired during and after birth.

microbiology↗

bioRxiv2019

Outwitting planarians antibacterial defence mechanisms: Rickettsiales bacterial trans-infection from Paramecium multimicronucleatum to planarians

Most of the microorganisms belonging to genera responsible for vector-borne diseases (VBD) have hematophagous arthropods as vector/reservoir. Recently, many new species of microorganisms phylogenetically related to agents of VBD were found in a variety of aquatic eukaryotic hosts, in particular, numerous new bacterial species related to the genus Rickettsia (Alphaproteobacteria, Rickettsiales) were discovered in protist ciliates and other unicellular eukaryotes. Although their pathogenicity for humans and terrestrial animals is not known, these bacteria might act as etiological agents of possible VBD of aquatic organisms, with protist as vectors. In the present study, we characterized a novel strain of the Rickettsia-Like Organism (RLO) endosymbiont \"Candidatus (Ca.) Trichorickettsia mobilis\" in the macronucleus of the ciliate Paramecium multimicronucleatum through Fluorescence In Situ Hybridization (FISH) and molecular analyses. Ultrastructural investigations on the presence of flagella confirmed previous studies on the same bacterial species. The potential trans-infection per os of this bacterium to planarians (Dugesia japonica), a widely used model system able to eliminate a wide range of bacteria pathogenic to humans and other Metazoa, was further verified. Ciliate mass cultures were set up, and trans-infection experiments were performed by adding homogenized paramecia to food of antibiotic-treated planarians, performed. Treated and non-treated (i.e. control) planarians were investigated at day 1, 3, and 7 after feeding for endosymbiont presence by means of PCR and ultrastructural analyses. Obtained results were fully concordant and suggest that this RLO endosymbiont can be transferred from ciliates to metazoans, being detected up to day 7 in treated planarian enterocytes inside and, possibly, outside phagosomes.

microbiology↗

bioRxiv2018

The Sicilian wolf: genetic identity of a recently extinct insular population

During historical times many local grey wolf (Canis lupus) populations underwent a substantial reduction of their sizes or became extinct. Among these, the wolf population once living in Sicily, the biggest island of the Mediterranean Sea, was completely eradicated by human persecution in the early decades of the XX century.\n\nIn order to understand the genetic identity of the Sicilian wolf, we applied ancient DNA techniques to analyse the mitochondrial DNA of six specimens actually stored in Italian museums.\n\nWe successfully amplified a diagnostic mtDNA fragment of the control region (CR) in four of the samples. Results showed that two samples shared the same haplotype, that differed by two substitutions from the currently most diffused Italian wolf haplotype (W14) and one substitution from the only other Italian haplotype (W16). The third sample showed a wolf-like haplotype never described before and the fourth a haplotype commonly found in dogs.\n\nFurthermore, all the wolf haplotypes detected in this study belonged to the mitochondrial haplogroup that includes haplotypes detected in all the known European Pleistocene wolves and in several modern southern European populations.\n\nUnfortunately, this endemic island population, bearing unique mtDNA variability, was definitively lost before it was possible to understand its taxonomic uniqueness and conservational value.

genetics↗