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Almeida, F.

Publications and source records attributed to Almeida, F..

3 recordsLinked to original sources

What does mitogenomics tell us about the evolutionary history of the Drosophila buzzatii cluster (repleta group)

The Drosophila repleta group is an array of more than 100 cactophilic species endemic to the \"New World\". The acquisition of the ability to utilize decaying cactus tissues as breeding and feeding sites is a key aspect that allowed the successful diversification of the repleta group in the American deserts. Within this group, the Drosophila buzzatii cluster is a South American clade of seven cactophilic closely related species in different stages of divergence, a feature that makes it a valuable model system for evolutionary research. However, even though substantial effort has been devoted to elucidating the phylogenetic relationships among members of the D. buzzatii cluster, the issue is still controversial. In effect, molecular phylogenetic studies performed to date generated ambiguous results since tree topologies depend on the kind of molecular marker employed. Curiously, even though mitochondrial DNA has become a popular marker in evolutionary biology and population genetics, none of the more than twenty Drosophila mitogenomes assembled so far belongs to this cluster. In this work we report the assembly of six complete mitogenomes of five species: D. antonietae, D. borborema, D. buzzatii, D. seriema and two strains of D. koepferae, with the aim to revisit the phylogenetic relationships and divergence times by means of a mitogenomic approach. The recovered topology using complete mitogenomes gives support to the hypothesis of the monophyly of that the D. buzzatii cluster and shows two main clades, one including D. buzzatii and D. koepferae (both strains) and the other the remaining species. These results are in agreement with previous reports based on a few mitochondrial and/or nuclear genes but in conflict with the results of a recent large-scale nuclear phylogeny, suggesting that nuclear and mitochondrial genomes depict different evolutionary histories.

evolutionary biology

Galectin-3 inhibits Paracoccidioides brasiliensis growth and impacts paracoccidioidomycosis through multiple mechanisms

The thermodimorphic pathogenic fungi Paracoccidioides brasiliensis and Paracoccioidioides lutzii are the etiologic causes of paracoccidioidomycosis (PCM), the most prevalent systemic mycosis in Latin America. Galectin-3 (Gal-3), an animal {beta}-galactoside-binding protein, modulates important roles during microbial infections, such as triggering a Th2-polarized immune response in PCM. Herein, we demonstrate that Gal-3 also plays other important roles in P. brasiliensis infection. We verified Gal-3 levels are upregulated in human and mice infections and establish that Gal-3 inhibits P. brasiliensis growth by inhibiting budding. Furthermore, Gal-3 affects disruption and internalization of extracellular vesicles (EV) from P. brasiliensis by macrophages. Our results suggest important roles for Gal-3 in P. brasiliensis infection, indicating that increased Gal-3 production during P. brasiliensis infection may account for affecting the fungal growth and EV stability, promoting a benefic course of experimental PCM. IMPORTANCEParacoccidiodomycosis (PCM) is the most prevalent systemic mycosis in Latin America. Although the immune mechanisms to control PCM are still not fully understood, several events of the host innate and adaptive immunity are crucial to determine the progress of the infection. Mammalian {beta}-galactoside-binding protein Galectin-3 (Gal-3) plays significant roles during microbial infections, and has been studied for its immunomodulatory roles but it can also have direct antimicrobial effects. We asked whether this protein plays a role in P. brasiliensis. We report herein that Gal-3 indeed has direct effects on fungal pathogen, inhibiting fungal growth and reducing extracellular vesicles stability. Our results suggest a direct role for Gal-3 in P. brasiliensis infection, with beneficial effects for the mammalian host.

microbiology

Postnatal development of skeletal muscle in IUGR pigs: morphofunctional phenotype and molecular mechanisms

Intrauterine growth restriction (IUGR) is a serious condition which impairs the achievement of the fetus full growth potential and occurs in a natural and severe manner in pigs. Knowledge on skeletal muscle morphofunctional phenotype and its molecular regulation in IUGR pigs is important to understand postnatal muscle development and may help the establishment of therapies to improve skeletal muscle growth in those individuals. To investigate the impairment of skeletal muscle postnatal development due to IUGR, we evaluated the histomorphometrical pattern of the semitendinosus muscle, the Myosin Heavy Chain (embryonic, I, IIa, IIb and IIx MyHC) fiber composition and the relative expression of genes related to myogenesis, adipogenesis and growth during three specific periods: postnatal myogenesis (newborn to 100 days of age), postnatal development (newborn to 150 days of age), and hypertrophy (100 days to 150 days of age), comparing IUGR and normal birth weight (NW) pigs. Growth restriction in utero affected muscle fiber diameter, total fiber number and muscle cross sectional area which were smaller in IUGR pigs at birth (P < 0.05). Even though the percentage of MyHC-I myofibers was higher in IUGR females at birth (P < 0.05), in older gilts, a lower percentage of MyHC-IIx isoform (P < 0.05) and the presence of emb-MyHC were also observed in that experimental group. Regarding the pattern of gene expression in the postnatal myogenesis period, growth restriction in utero led to a down regulation of myogenic factors, which delayed the expression of signals that induces skeletal muscle myogenesis (PAX7, MYOD, MYOG, MYF5 and DES). Taken together, the muscle morphofunctional aspects described and their ontogenetic regulation define the possible molecular origins of the notorious damage to the postnatal musculature development in IUGR pigs.

cell biology