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De Pitta, C.

Publications and source records attributed to De Pitta, C..

7 recordsLinked to original sources

Integrating morphological and molecular approaches to assess photosynthetic species diversity in the Venice Lagoon

The Venice Lagoon is the largest transitional environment in the Mediterranean Sea and an important biodiversity hotspot. However, it is under increasing climate and anthropogenic pressures, highlighting the need for long-term monitoring of its biodiversity. Three monitoring campaigns were conducted between 2023 and 2025, sampling seaweeds, seagrasses and halophytes. Samples were identified using an integrated morphological and molecular approach, with morphological traits guiding the selection of the most appropriate DNA-barcoding markers. High-quality sequences were obtained for 50% of the samples and compared with reference databases. To improve identification reliability, phylogenetic trees were reconstructed for each major taxonomic group to assess clustering patterns and sequence relationships. Two independent species-delimitation methods, ASAP and GMYC, were also applied. Overall, 81 taxa were identified, 13 belonging to Chlorophyta, 11 to Heterokontophyta, 28 to Rhodophyta, and 29 to Tracheophyta. We further conducted a targeted survey on Sporobolus species using the trnL-trnF marker and genome-size estimates to distinguish between native and non-indigenous ones. The presence of S. x townsendii was confirmed in the central and southern lagoon, while the non-indigenous S. anglicus was more prevalent than the native S. maritimus.

ecology↗

Grass wars: how native and non-indigenous Sporobolus battle heatwaves in salt marshes

O_LIHeatwaves are increasing in frequency and intensity and may alter competitive interactions between native and non-indigenous plant species. C_LIO_LIWe compared the responses of the native Sporobolus maritimus and the non-indigenous Sporobolus anglicus to a simulated 5-day heatwave using an integrative approach combining morphological, physiological, biochemical, transcriptomic, and metabolomic analyses. C_LIO_LIS. maritimus showed reduced survival, greater physiological damage, and no recovery, indicating high sensitivity to heat stress. Conversely, S. anglicus exhibited a rapid and coordinated response, limited damage to the photosynthetic apparatus, and full recovery after stress. C_LIO_LIThese results highlight the greater resilience of S. anglicus and suggest a potential decline of the native species in the Venetian salt marshes under increasing heat stress. C_LI Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=139 SRC="FIGDIR/small/728445v1_ufig1.gif" ALT="Figure 1"> View larger version (49K): org.highwire.dtl.DTLVardef@1579ffeorg.highwire.dtl.DTLVardef@1c8e490org.highwire.dtl.DTLVardef@15cbadorg.highwire.dtl.DTLVardef@ef024b_HPS_FORMAT_FIGEXP M_FIG C_FIG We investigated the effects of heatwaves on a native and NIS Sporobolus species from the Venice Lagoon using an integrative, multi-level approach during a simulated 5-day heatwave and recovery phase. The native species showed reduced survival, pronounced physiological damage, and no recovery, indicating high sensitivity to heat stress. Conversely, the NIS exhibited a rapid response, limited impairment of the photosynthetic apparatus, and full recovery. These findings indicate greater resilience of the NIS and suggest a potential decline of the native species in the Venice Lagoon under increasing heat stress. Image created with BioRender (www.biorender.com).

plant biology↗

RNase H1 counteracts DNA damage and ameliorates SMN-dependent phenotypes in a Drosophila model of Spinal Muscular Atrophy

Spinal Muscular Atrophy (SMA) is caused by a deficiency of the Survival Motor Neuron (SMN) protein. Mutations in SMN disrupt mRNA splicing and translation, leading to maladaptive changes in transcriptomes, proteomes, neuroinflammation, and metabolism, which drive motor neuron degeneration in SMA patients. Using a Drosophila SMA model, we found that systemic depletion of Smn leads to accumulation of RNA:DNA hybrids (R-loops), increased DNA damage, dysregulation of amino acids and sugar metabolism and activation of the innate immune response, recapitulating key pathological features reported in mammalian models and severe SMA patients. Persistent DNA damage in Smn-deficient flies alters cell proliferation rates in larval brains and induces extensive cell death in the developing eye. Importantly here, we show that stimulating the resolution of RNA:DNA hybrids with transgenic human RNAse H1 prevents the accumulation of DNA damage and attenuates the transcriptome and amino acid alterations induced by Smn depletion, mitigating the Smn-dependent cellular and developmental abnormalities, in Smn-deficient flies. Our data suggest that depletion of Smn causes an accumulation of aberrant transcripts and chronic DNA damage, which--along with the altered metabolomic profiles associated with Smn deficiency--trigger systemic inflammatory responses, ultimately affecting neuronal function and survival.

genetics↗

miR-210 is essential to retinal homeostasis in fruit flies and mice

miR-210 is one of the most evolutionarily conserved microRNAs. Recent studies in Drosophila melanogaster have unveiled that the absence of miR-210 leads to a progressive retinal degeneration characterized by the accumulation of lipid droplets and disruptions in lipid metabolism. Further investigation into lipid anabolism and catabolism revealed significant alterations in gene expression within these pathways. We provide the first morphological characterization of miR-210 KO mice retinas, highlighting a significant photoreceptor degeneration. While exploring potential parallels between miR-210 KO models in flies and mice, we examined mice lipid metabolism, circadian behaviour, and retinal transcriptome yet found no resemblances, suggesting divergent mechanisms of retinal degeneration between the two species. Simultaneously, analysis of the transcriptome in the brains of miR-210 KO flies revealed the potential existence of a shared upstream mechanism contributing to retinal degeneration in both fruit flies and mammals.

genetics↗

Low dose/dose rate γ irradiation protects Drosophila melanogaster chromosomes from double strand breaks and telomere fusions by modulating the expression of Loquacious.

It is still continuously debated whether the low-dose/dose-rate (LDR) of ionizing radiation represents a hazard for humans. Model organisms, such as fruit flies, are considered valuable systems to reveal insights into this issue. We found that, in wild-type Drosophila melanogaster larval neuroblasts, the frequency of Chromosome Breaks (CBs), induced by acute {gamma}-irradiation, is significantly reduced when flies are previously exposed to a protracted dose of 0.4Gy delivered at a dose rate of 2.5mGy/h. This indicates that this exposure, which is associated with an increased expression of DNA damage response proteins, induces a radioadaptive response (RAR) that protects Drosophila from extensive DNA damage. Interestingly, the same exposure reduces the frequency of telomere fusions (TFs) from Drosophila telomere capping mutants suggesting that the LDR can generally promote a protective response on chromatin sites that are recognized as DNA breaks. Deep RNA sequencing revealed that RAR is associated with a reduced expression of Loquacious D (Loqs-RD) gene that encodes a well-conserved dsRNA binding protein required for esiRNAs biogenesis. Remarkably, loss of Loqs mimics the LDR-mediated chromosome protection as it decreases the IR-induced CBs and TF frequency. Thus, our molecular characterization of RAR identifies Loqs as a key factor in the cellular response to LDR and unveils unprecedented epigenetic routes involved in radioresistance.

genetics↗

The most comprehensive annotation of the Krill transcriptome provides new insights for the study of physiological processes and environmental adaptation

The krill species Euphausia superba plays a critical role in the food chain of the Antarctic ecosystem, as the abundance of its biomass affects trophic levels both below it and above. Major changes in climate conditions observed in the Antarctic Peninsula region in the last decades have already altered the distribution of the krill population and its reproductive dynamics. A deeper understanding of the adaptation capabilities of this species, and of the molecular mechanisms behind it are urgently needed. The availability of a large body of RNA-seq assays gave us the opportunity to extend the current knowledge of the krill transcriptome, considerably reducing errors and redundancies. Our study covered the entire developmental process, from larval stages to adult individuals, providing information of central relevance for ecological studies. Here we describe the KrillDB2 database, a resource combining the latest annotation of the krill transcriptome with a series of analyses specifically targeting genes and molecular processes relevant to krill physiology. KrillDB2 provides in a single resource the most complete collection of experimental data and bioinformatic annotations: it includes an extended catalog of krill genes; an atlas of their expression profiles over all RNA-seq datasets publicly available; a study of differential expression across multiple conditions such as developmental stages, geographical regions, seasons, and sexes. Finally, it provides initial indications about non-coding RNAs, a class of molecules whose contribute to krill physiology has never been reported before.

ecology↗

TGS1 controls snRNA 3' end processing, prevents neurodegeneration and ameliorates SMN-dependent neurological phenotypes in vivo

Trimethylguanosine synthase 1 (TGS1) is a highly conserved enzyme that converts the 5 mono-methylguanosine cap of snRNAs to a trimethylguanosine cap. Here, we show that loss of TGS1 in C. elegans, D. melanogaster and D. rerio results in neurological phenotypes similar to those caused by Survival Motor Neuron (SMN) deficiency. Importantly, expression of human TGS1 ameliorates the SMN-dependent neurological phenotypes in both flies and worms, revealing that TGS1 can partly counteract the effects of SMN deficiency. TGS1 loss in HeLa cells leads to the accumulation of immature U2 and U4atac snRNAs with long 3 tails that are often uridylated. snRNAs with defective 3 terminations also accumulate in Drosophila Tgs1 mutants. Consistent with defective snRNA maturation, TGS1 and SMN mutant cells also exhibit partially overlapping transcriptome alterations that include aberrantly spliced and readthrough transcripts. Together, these results identify a neuroprotective function for TGS1 and reinforce the view that defective snRNA maturation affects neuronal viability and function.

genetics↗