Biology subjects

Andreani, C.

Publications and source records attributed to Andreani, C..

4 recordsLinked to original sources

bioRxiv2026

Satellite-gene abundance fusion reveals global hotspots of ocean ecosystem services

The Ocean sustains planetary health through climate regulation, biodiversity, and essential ecosystem services. Plankton underpins these processes by driving primary production, sustaining food webs, and mediating carbon sequestration. Yet the spatial organization of plankton-based ecosystem services remains poorly understood. The High Seas Treaty and the 30% Ocean protection target by 2030 create an urgent need for science-based guidance for global ocean governance. Here, we aim to identify key planktonic areas associated with functional diversity, net primary productivity, and carbon export globally. We used machine learning to integrate omics-derived plankton functions and satellite observations with diversity metric and ecosystem services. Leveraging metagenomic data, we identified molecular functions strongly linked to ecosystem functioning and project their global distributions across seasons. We reveal putative hotspots of functional diversity, net primary productivity, and carbon export. Our analysis pinpoints areas where all three indicators converge synchronously, predominantly along oceanographic structures such as polar fronts and principal current systems. By relying on satellite data as core input, our approach captures the temporal variability of these hotspots, providing a global, dynamic protocol for projections of plankton-based ecosystem services. These findings establish a foundation for developing integrative conservation tools based on ecosystem functioning and inform adaptive management under climate change.

ecology↗

bioRxiv2025

Thioredoxin Reductase 1 inhibition triggers ferroptosis in KRAS-independent lung cancers

Lung cancers that harbor wild type KRAS (KRAS-WT) represent a molecularly diverse subset of tumors that often lack targeted therapeutic options. Using synthesized gold(I)-based inhibitors, a multi-omics approach, and functional validation, we identified Thioredoxin reductase 1 (TXNRD1), encoding as a selective vulnerability in KRAS-WT and oncogenic KRAS mutant (KM)-independent lung cancer (LC). Mechanistically, TRXR1 blockade induces ferroptosis through glutathione depletion, lipid reactive oxygen species (ROS) accumulation, and HMOX1-dependent iron overload in KRAS-WT LC both in vitro and in vivo. Furthermore, while KM LC cells are intrinsically resistant to TRXR1 inhibition, KMLC cells that acquire resistance to KRAS inhibitors (KRASi) undergo a redox shift that renders them sensitive to TRXR1 inhibition, uncovering a potential novel therapeutic vulnerability in KRASi-refractory tumors. These findings establish TRXR1 as a targetable redox checkpoint in KRAS-WT and KRASi-resistant lung cancers and support further development of TRXR1 inhibitors.

cancer biology↗

bioRxiv2025

Planetary-scale marine community modeling predicts metabolic synergy and viral impacts

The oceans buffer against climate change via biogeochemical cycles underpinned by microbial metabolic activities. While planetary-scale surveys provide baseline microbiome data, inferring metabolic and biogeochemical impacts remains challenging. Genome-scale modeling has addressed analogous issues at the cellular level, highlighting key metabolic reactions contingent upon specific environmental conditions. Here we adapt this mechanistic modeling framework towards analyzing global ocean microbial communities to reveal metabolic processes predicted to maintain ecosystem functioning. To achieve this, we developed a genome-scale superorganism metabolic model for each TARA Ocean metagenome or metatranscriptome (i.e., limited to reactions known from heterotrophic prokaryotes and viruses), and evaluated these models to establish a community-wide metabolic phenotype for each sample. To validate, we showed that even with reaction-mappable genes only ([~]1/4 of the total genes), model composition revealed metabolism-inferred ecological zones that matched taxonomy-inferred zones. Model inferred metabolic phenotypes revealed reaction cooperation associated with microbial metabolism and organism diversity. These phenotypes also suggest elevated ecological roles for viruses as model predictions suggest they genomically target community-critical metabolic reactions that underpin metabolic phenotype stability, and also demonstrate that, as metabolites are better understood, immediate estimates could be made for where viruses remineralize versus sink carbon. While this new constraints-based, agile, and mechanistic modeling framework is highly upgradable, it already begins to convert molecular-scale environmental omics data to ecological and even planetary-scale biogeochemical features that will better bring microbes and their viruses into Earth system and climate models.

systems biology↗

bioRxiv2021

Targeting de novo lipogenesis and the Lands cycle induces ferroptosis in KRAS-mutant lung cancer

Mutant KRAS (KM) is the most common oncogene in lung cancer (LC). KM regulates several metabolic networks, but their role in tumorigenesis is still not sufficiently characterized to be exploited in cancer therapy. To identify metabolic networks specifically deregulated in KMLC, we characterized the lipidome of genetically engineered LC mice, cell lines, patient derived xenografts and primary human samples. We also determined that KMLC, but not EGFR-mutant (EGFR-MUT) LC, is enriched in triacylglycerides (TAG) and phosphatidylcholines (PC). We also found that KM upregulates fatty acid synthase (FASN), a rate-limiting enzyme in fatty acid (FA) synthesis promoting the synthesis of palmitate and PC. We determined that FASN is specifically required for the viability of KMLC, but not of LC harboring EGFR-MUT or wild type KRAS. Functional experiments revealed that FASN inhibition leads to ferroptosis, a reactive oxygen species (ROS)-and iron-dependent cell death. Consistently, lipidomic analysis demonstrated that FASN inhibition in KMLC leads to accumulation of PC with polyunsaturated FA (PUFA) chains, which are the substrate of ferroptosis. Integrating lipidomic, transcriptome and functional analyses, we demonstrated that FASN provides saturated (SFA) and monounsaturated FA (MUFA) that feed the Lands cycle, the main process remodeling oxidized phospholipids (PL), such as PC. Accordingly, either inhibition of FASN or suppression of the Lands cycle enzymes PLA2 and LPCAT3, promotes the intracellular accumulation of lipid peroxides and ferroptosis in KMLC both in vitro and in vivo. Our work supports a model whereby the high oxidative stress caused by KM dictates a dependency on newly synthesized FA to repair oxidated phospholipids, establishing a targetable vulnerability. These results connect KM oncogenic signaling, FASN induction and ferroptosis, indicating that FASN inhibitors already in clinical trial in KMLC patients (NCT03808558) may be rapidly deployed as therapy for KMLC.

cancer biology↗