Biology subjects

Melo, T.

Publications and source records attributed to Melo, T..

6 recordsLinked to original sources

bioRxiv2025

Preservation and remodelling of chloroplast lipids in photosynthetic sea slug host cells

The capacity to retain long-term functional algal chloroplasts within animal cells is a singular trait of some Sacoglossa sea slugs. The stolen chloroplasts (kleptoplasts) confer photosynthetic capacity to the host. This study investigated how chloroplast lipidomes from two macroalgae (Acetabularia acetabulum and Bryopsis sp.) are modified after sequestration by the photosynthetic sea slugs Elysia crispata, Elysia viridis, and Elysia timida. Pigments were analysed by HPLC, and lipidomic profiling of chloroplasts (glycolipids, betaine lipids, phytosterols) was conducted using C18-LC-MS/MS. Kleptoplasts retain intact algal pigment profile. Glycolipid signatures in sea slug tissues closely resembled those of their algal donors, although shifts in relative abundances suggest remodelling of plastidial membranes, potentially affecting kleptoplast morphology, particularly membrane curvature and stability. In contrast, betaine lipid composition differed markedly between sea slugs and algal donors, with major betaine species common to all sea slugs. Phytosterol composition was better preserved in sea slugs feeding on Bryopsis sp. than on A. acetabulum. This study demonstrated that kleptoplast lipidomes maintain a strong algal identity but undergo selective modifications within the animal host. This remodelling likely optimizes membrane architecture to support long-term stability and photosynthetic functionality within the hosts cellular environment, facilitating the integration and performance of sea slug kleptoplasts. HighlightThe lipid profiles of photosynthetic sea slugs resemble the algal donors chloroplasts. However, alterations in glycolipid composition suggest that the molecular architecture of kleptoplasts is modulated by the host cells.

biochemistry↗

bioRxiv2025

Lipid droplet dysmetabolism affects cell homeostasis in an in vitro model of Alzheimer disease

Lipid droplets (LD) are dynamic organelles involved in neutral lipid storage, energy homeostasis, and can prevent lipotoxicity and oxidative distress. LD dysmetabolism has been considered a pathological hallmark in neurodegenerative disorders, including Alzheimers disease (AD). In this study, we investigated the alterations in LD metabolism and their impact on mitochondria-associated membranes (MAM) in an in vitro model of AD, namely the mouse neuroblastoma cell (N2A) line overexpressing the amyloid precursor protein with the familial Swedish mutation (APPswe). In APPswe cells, we found depletion of LD associated with an accumulation of free fatty acids that can be related with the observed LD degradation by chaperone-mediated autophagy. In these cells we also found decreased levels of seipin, which might contribute to triacylglycerol accumulation. These lipid alterations are associated with increased levels of ROS and lipid peroxidation in APPswe cells. The pharmacological modulation of DGAT1, that mediates triacylglycerol synthesis, normalized LD size and improved ER-mitochondria contacts and mitochondrial function in APPswe cells. In summary, these observations suggest the involvement of altered LD metabolism in AD pathophysiology, which impact on MAM and mitochondria function leading to cell dyshomeostasis. Our findings also support the idea that LD are relevant therapeutic targets in AD. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=111 SRC="FIGDIR/small/658644v1_ufig1.gif" ALT="Figure 1"> View larger version (41K): org.highwire.dtl.DTLVardef@de3fc6org.highwire.dtl.DTLVardef@12d1f2forg.highwire.dtl.DTLVardef@15a5185org.highwire.dtl.DTLVardef@9e1655_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2021

Molecular programming in utero modulates hepatic lipid metabolism and adult metabolic risk in obese mother offspring in a sex-specific manner

Male and female offspring of obese mothers are known to differ significantly in their metabolic adaptation and later development of complications. We investigated the sex-dependent responses in obese offspring of mice with maternal obesity, focusing on changes in liver glucose and lipid metabolism. Maternal obesity prior to and during gestation led to hepatic insulin resistance and inflammation in male offspring, while female offspring were protected. These sex differences were explained by more efficient transcriptional and posttranscriptional reprogramming of metabolic pathways to prevent the damaging effects of maternal obesity in females compared to males. These differences were sustained later in life, resulting in a better metabolic balance in female offspring. In conclusion, sex and maternal obesity drive transcriptional and posttranscriptional regulation of major metabolic processes in offspring liver differently, explaining the sexual dimorphism in obesity-associated metabolic risk.

physiology↗

bioRxiv2021

Maternal obesity programs white and brown adipose tissue transcriptome and lipidome in offspring in a sex-dependent manner

The prevalence of overweight and obesity among children has drastically increased during the last decades and maternal obesity has been demonstrated as one of the ultimate factors. Nutrition-stimulated transgenerational epigenetic regulation of key metabolic genes is fundamental to the developmental origins of the metabolic syndrome. Fetal nutrition may differently influence female and male offspring. In this work, we investigated the sex-dependent programming of maternal obesity in visceral, subcutaneous and brown adipose tissues of offspring using magnetic resonance imaging and spectroscopy and a lipidomic approach combined with a Smart-Seq2 differential sequencing analysis. We show that the triglyceride profile varies between adipose depots, sexes and maternal diet. Our results demonstrate for the first time that a sex-dependent gene programming exists in visceral, subcutaneous and brown adipose tissues. Maternal obesity differentially programs gene expression in adipose depots of female and male offspring, which may contribute to the sex-dependent metabolic complications later in life. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=146 SRC="FIGDIR/small/430188v1_ufig1.gif" ALT="Figure 1"> View larger version (34K): org.highwire.dtl.DTLVardef@8ceac8org.highwire.dtl.DTLVardef@18a2a32org.highwire.dtl.DTLVardef@1d8530dorg.highwire.dtl.DTLVardef@1349512_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

bioRxiv2021

Cholesteryl Hemiazelate Induces Lysosome Dysfunction and Exocytosis in Macrophages

OBJECTIVEA key event in atherogenesis is the formation of lipid-loaded macrophages, lipidotic cells, which exhibit irreversible accumulation of undigested modified low-density lipoproteins in lysosomes. This event culminates with the loss of cell homeostasis, inflammation and cell death. In this study we propose to identify the chemical etiological factors and understanding the molecular and cellular mechanisms responsible for the impairment of lysosome function in macrophages. APPROACH AND RESULTSUsing shotgun lipidomics we have discovered that a family of oxidized lipids (cholesteryl hemiesters, ChE), end products of oxidation of polyunsaturated cholesteryl esters, occurs at higher concentrations in the plasma of two cohorts of cardiovascular disease patients than in the plasma of a control cohort. Macrophages exposed to the most prevalent ChE, cholesteryl hemiazelate (ChA) exhibit lysosome enlargement, peripheral lysosomal positioning, lysosome dysfunction and lipidosis which are irreversible. The transcriptomic profile of macrophages exposed to ChA indicates that the lysosome pathway is deeply affected and is well correlated with lysosome phenotypic and functional changes. Interestingly, the dysfunctional peripheral lysosomes are more prone to fuse with the plasma membrane, secreting their undigested luminal content into the extracellular milieu with potential consequences to the pathology. CONCLUSIONWe identify ChA not only as one of the molecules involved in the etiology of irreversible lysosome dysfunction culminating with lipidosis but also as a promoter of exocytosis of the dysfunctional lysosomes. The latter event is a new mechanism that may be important in the pathogenesis of atherosclerosis.

cell biology↗

bioRxiv2020

Genetics survey reveals colonization and philopatry of the loggerhead sea turtles across geographic scales

AimUnderstanding the processes that underlie the distribution of genetic diversity in endangered species is a goal of modern conservation biology. Specifically, how population structure affects genetic diversity and contributes to a species adaptive potential remain elusive. The loggerhead sea turtle (Caretta caretta) faces multiple conservation challenges due to its migratory nature and philopatric behaviour. LocationsAtlantic Ocean, Cabo Verde, island of Boavista MethodsHere, using 4207 mtDNA sequences, we analysed the colonisation patterns and distribution of genetic diversity within a major ocean basin (the Atlantic), a regional rookery (Cabo Verde Archipelago) and a local island (Island of Boavista, Cabo Verde). ResultsHypothesis-driven population genetic models suggest the colonization of the Atlantic has occurred in two distinct waves, each corresponding to major mtDNA lineages. We propose the oldest lineage entered the basin via the isthmus of Panama and sequentially established aggregations in Brazil, Cabo Verde and in the area of USA and Mexico. The second lineage entered the Atlantic via the Cape of Good Hope, establishing colonies in the Mediterranean Sea, and from then on, re-colonized the already existing rookeries of the Atlantic. At the Cabo Verde level, we reveal an asymmetric gene flow maintaining links across nesting groups despite significant genetic structure amongst nesting groups. This structure stems from female philopatric behaviour which could further be detected by weak but significant structure amongst beaches separated by only a few kilometres on the island of Boavista. Main conclusionTo explore demographic processes at diverse geographic scales improves understanding the complex evolutionary history of highly migratory philopatric species. Unveiling the past facilitates the design of conservation programmes targeting the right management scale to maintain a species adaptive potential and putative response to human-induced selection.

evolutionary biology↗