Biology subjects

Rizzuto, G.

Publications and source records attributed to Rizzuto, G..

4 recordsLinked to original sources

bioRxiv2023

The invasive brown seaweed Rugulopteryx okamurae (Dictyotales, Ochrophyta) continues to expand: first record in Italy.

The brown seaweed Rugulopteryx okamurae (Dictyotales, Ochrophyta), native to the Pacific Ocean and widely distributed in Asia, has been recently recognized as an emblematic case of biological invasion by marine macroalgae in European waters. Since 2015 and from the Strait of Gibraltar, R. okamurae has rapidly spread towards Atlantic and Mediterranean coastal areas exhibiting an invasive behaviour with significant ecological and economic impacts. Here, we report by morphology and genetics the first observation of this species in Italy along the north-western coast of Sicily (Gulf of Palermo), as drifted material and an established population on Posidonia oceanica, representing its new eastern distribution limit in the Mediterranean Sea, previously established in Marseilles (France). Furthermore, we have performed with the current introduced distribution of the species a favorability distribution model for the Mediterranean, which shows most of the western Mediterranean, including the Balearic archipelago, Corsica and Sardinia, central Mediterranean, including Sicily, and the northern coast of Africa together with eastern Mediterranean basin, as highly favorable for R. okamurae. Arrival of the species into this new area is suggested by means of sea currents and maritime traffic, including fishing activities, hypothesis supported by some of the ranked variables that entered the favorability model, i.e, current velocity, and proximity of fishing ports. These results are a warning that the species can cover large sea distances favored by sea currents, thus also threatening the ecosystems and marine resources of the central and eastern Mediterranean, highly favorable regions for the species. We suggest coordinated actions at the European level regarding prevention, among which those that have the complicity of the fishing sector should be considered, both because it is a highly affected sector and because it potentially has a very important role in the dispersion of the species.

plant biology↗

bioRxiv2023

Validation of a murine proteome-wide phage display library for the identification of autoantibody specificities

Autoimmunity is characterized by loss of tolerance to tissue-specific as well as systemic antigens, resulting in complex autoantibody landscapes. Here, we introduce and extensively validate the performance characteristics of a murine proteome-wide library for phage display immunoprecipitation and sequencing (PhIP-seq), to profile mouse autoantibodies. This system and library were validated using seven genetic mouse models across a spectrum of autoreactivity. Mice deficient in antibody production (Rag2-/- and MT) were used to model non-specific peptide enrichments, while cross-reactivity was evaluated using anti-ovalbumin B cell receptor (BCR)-restricted OB1 mice as a proof of principle. The PhIP-seq approach was then utilized to interrogate three distinct autoimmune disease models. First, serum from Lyn-/- IgD+/- mice with lupus-like disease was used to identify nuclear and apoptotic bleb reactivities, lending support to the hypothesis that apoptosis is a shared origin of these antigens. Second, serum from non-obese diabetic (NOD) mice, a polygenic model of pancreas-specific autoimmunity, enriched peptides derived from both insulin and predicted pancreatic proteins. Lastly, Aire-/- mouse sera were used to identify numerous auto-antigens, many of which were also observed in previous studies of humans with autoimmune polyendocrinopathy syndrome type 1 (APS1) carrying recessive mutations in AIRE. Among these were peptides derived from Perilipin-1, a validated autoimmune biomarker of generalized acquired lipodystrophy in humans. Autoreactivity to Perilipin-1 correlated with lymphocyte infiltration in adipose tissue and underscores the approach in revealing previously unknown specificities. These experiments support the use of murine proteome-wide PhIP-seq for antigenic profiling and autoantibody discovery, which may be employed to study a range of immune perturbations in mouse models of autoimmunity.

immunology↗

bioRxiv2021

Spatio-temporal coordination at the maternal-fetal interface promotes trophoblast invasion and vascular remodeling in the first half of human pregnancy

Beginning in the first trimester, fetally derived extravillous trophoblasts (EVTs) invade the uterus and remodel its spiral arteries, transforming them into large, dilated blood vessels left with a thin, discontinuous smooth muscle layer and partially lined with EVTs. Several mechanisms have been proposed to explain how EVTs coordinate with the maternal decidua to promote a tissue microenvironment conducive to spiral artery remodeling (SAR). However, it remains a matter of debate which immune and stromal cell types participate in these interactions and how this process evolves with respect to gestational age. Here, we used a multiomic approach that combined the strengths of spatial proteomics and transcriptomics to construct the first spatiotemporal atlas of the human maternal-fetal interface in the first half of pregnancy. We used multiplexed ion beam imaging by time of flight (MIBI-TOF) and a 37-plex antibody panel to analyze [~]500,000 cells and 588 spiral arteries within intact decidua from 66 patients between 6-20 weeks of gestation, integrating this with coregistered transcriptomic profiles. Gestational age substantially influenced the frequency of many maternal immune and stromal cells, with tolerogenic subsets expressing CD206, CD163, TIM-3, Galectin-9, and IDO-1 increasingly enriched and colocalized at later time points. In contrast, SAR progression preferentially correlated with EVT invasion and was transcriptionally defined by 78 gene ontology pathways exhibiting unique monotonic and biphasic trends. Lastly, we developed an integrated model of SAR supporting an intravasation mechanism where invasion is accompanied by upregulation of pro-angiogenic, immunoregulatory EVT programs that promote interactions with vascular endothelium while avoiding activation of immune cells in circulating maternal blood. Taken together, these results support a coordinated model of decidualization in which increasing gestational age drives a transition in maternal decidua towards a tolerogenic niche conducive to locally regulated, EVT-dependent SAR.

systems biology↗

bioRxiv2018

Listeria monocytogenes InlP interacts with afadin and facilitates basement membrane crossing

During pregnancy, the placenta protects the fetus against the maternal immune response, as well as bacterial and viral pathogens. Bacterial pathogens that have evolved specific mechanisms of breaching this barrier, such as Listeria monocytogenes, present a unique opportunity for learning how the placenta carries out its protective function. We previously identified the L. monocytogenes protein Internalin P (InlP) as a secreted virulence factor critical for placental infection (1). Here, we show that InlP, but not the highly similar L. monocytogenes internalin Lmo2027, binds to human afadin (encoded by AF-6), a protein associated with cell-cell junctions. A crystal structure of InlP reveals several unique features, including an extended leucine-rich repeat (LRR) domain with a distinctive Ca2+-binding site. Despite afadins involvement in the formation of cell-cell junctions, MDCK epithelial cells expressing InlP displayed a decrease in the magnitude of the traction stresses they could exert on deformable substrates, similar to the decrease in traction exhibited by AF-6 knock-out MDCK cells. L. monocytogenes {Delta}inlP mutants were deficient in their ability to form actin-rich protrusions from the basal face of polarized epithelial monolayers, a necessary step in the crossing of such monolayers (transcytosis). A similar phenotype was observed for bacteria expressing an internal in-frame deletion in inlP (inlP DLRR5) that specifically disrupts its interaction with afadin. However, afadin deletion in the host cells did not rescue the transcytosis defect. We conclude that secreted InlP targets cytosolic afadin to specifically promote L. monocytogenes transcytosis across the basal face of epithelial monolayers, which may contribute to the crossing of the basement membrane during placental infection.

microbiology↗