Biology subjects

Prado, F.

Publications and source records attributed to Prado, F..

6 recordsLinked to original sources

bioRxiv2026

Impact of Amazonian protected areas in preventing deforestation and carbon loss over four decades

Native vegetation protection is a key strategy for delivering both biodiversity and climate benefits, and protected areas have been widely adopted to keep tropical biomes standing. Yet deforestation is driven by interrelated environmental and social factors, and the effectiveness of protected areas varies considerably across space. Here, we evaluated the impact of 802 protected and conserved areas in the Brazilian Amazon on preventing vegetation loss and avoiding carbon emissions over the past 40 years using statistical matching to address the location bias of protection. We found that protected areas were effective throughout the study period, reducing the probability of deforestation per km2 by an average of 0.5 percentage points per year. While the Amazon biome lost 14% of its native vegetation between 1986 and 2024, protected areas prevented the deforestation of 290,436 km2, nine times their actual internal loss. They also stored 45,336 Mt of carbon in 2016 (61% of the Amazon stock) and prevented the emission of 7,300 Mt of CO2 by 2024. Deforestation inside the areas and remoteness reduced their impact, while areas that were initially more preserved were more effective. Area size and age had no influence over impact once we analyzed the amount of avoided deforestation per size and age. Impact also varied across Brazilian states, highlighting the role of regional context. All three protection categories (conservation units, indigenous lands, and quilombola territories) showed a positive mean impact, indicating that each, in aggregate, contributes to reducing deforestation. These findings provide robust evidence of the substantial role of Amazonian protected areas in habitat conservation and climate mitigation, while underscoring that this contribution remains undervalued. We advocate for strategically expanding protection to areas of greatest potential impact, and for securing adequate funding to ensure protected areas can fulfill that potential.

ecology↗

bioRxiv2024

Rad51 determines pathway usage in post-replication repair

Stalled replication forks can be processed by several distinct mechanisms collectively called post-replication repair which includes homologous recombination, fork regression, and translesion DNA synthesis. However, the regulation of the usage between these pathways is not fully understood. The Rad51 protein plays a pivotal role in maintaining genomic stability through its roles in HR and in protecting stalled replication forks from degradation. We report the isolation of separation-of-function mutations in Saccharomyces cerevisiae Rad51 that retain their recombination function but display a defect in fork protection leading to a shift in post-replication repair pathway usage from HR to alternate pathways including mutagenic translesion synthesis. Rad51-E135D and Rad51-K305N show normal in vivo and in vitro recombination despite changes in their DNA binding profiles, in particular to dsDNA, with a resulting effect on their ATPase activities. The mutants lead to a defect in Rad51 recruitment to stalled forks in vivo as well as a defect in the protection of dsDNA from degradation by Dna2-Sgs1 and Exo1 in vitro. A high-resolution cryo-electron microscopy structure of the Rad51-ssDNA filament at 2.4 [A] resolution provides a structural basis for a mechanistic understanding of the mutant phenotypes. Together, the evidence suggests a model in which Rad51 binding to duplex DNA is critical to control pathway usage at stalled replication forks.

molecular biology↗

bioRxiv2023

Ecological monitoring using Collembola metabarcoding with extremely low bycatch amplification.

Collembola are used widely to monitor soil health and functional parameters. Recent developments in high throughput sequencing (especially metabarcoding) have substantially increased their potential for these ends. Collembola are especially amenable to metabarcoding because of their small size, high abundance, and ubiquity in most habitat types. However, most Collembola sampling protocols collect a substantial and highly varied bycatch that can be a considerable impediment to metabarcoding, especially because of data lost to non-target species. We designed a primer set amplifying the D2 expansion segment of ribosomal DNA that is highly conserved across Collembola and successfully excludes from amplification nearly all other invertebrate taxa. We tested the diagnostic power of the primer set by clearly distinguishing Collembola communities between forest sites with differing habitat qualities in Sao Paulo State, Brazil. The oligos successfully amplified targets from all Collembola orders previously encountered in the sampling locations, with no non-target amplification, and also excluded the closely related Protura and Diplura. Alpha diversity (OTU count) and phylogenetic diversity was significantly higher in high quality habitats. Moreover, the beta diversity indices successfully differentiated high and low-quality habitats. This new addition to the biomonitoring toolbox greatly increases the accessibility of Collembola metabarcoding for various types of habitat assessments.

molecular biology↗

bioRxiv2022

Parental histone distribution at nascent strands controls homologous recombination during DNA damage tolerance

The advance and stability of replication forks rely on a tight co-regulation of the processes of DNA synthesis and nucleosome assembly. We have addressed the relevance of parental histone recycling in the mechanisms of DNA damage tolerance (DDT) - homologous recombination (HR) and translesion synthesis (TLS) - that assist replication forks under conditions that block their advance. We show that mutants affected in the deposition of parental histones are impaired in the recombinational repair of the single-strand DNA gaps generated during DDT, with the defects being more severe in mutants impaired in the lagging strand-specific deposition pathway. These recombinational defects are not due to a deficit of parental histones at the nascent strands but to an excess of parental nucleosomes at the invaded strand that destabilizes the sister chromatid junction formed after strand invasion. In conclusion, parental histone distribution at stressed forks regulates HR and provides a potential mechanism for the choice between HR and TLS that would depend on whether DNA synthesis is blocked at the lagging or the leading strand.

molecular biology↗

bioRxiv2020

Chromatin modifiers and recombination factors promote a telomere fold-back structure, that is lost during replicative senescence

Telomeres adopt a lariat conformation and hence, engage in long and short distance intra-chromosome interactions. Budding yeast telomeres were proposed to fold back into subtelomeric regions, but a robust assay to quantitatively characterize this structure has been lacking. Therefore, it is not well understood how the interactions between telomeres and non-telomeric regions are established and regulated. We employ a telomeric chromosome conformation capture (Telo-3C) approach to directly analyze telomere folding and its maintenance in S. cerevisiae. We identify the histone modifiers Sir2, Sin3 and Set2 as critical regulators for telomere folding, which suggests that a distinct telomeric chromatin environment is a major requirement for the folding of yeast telomeres. We demonstrate that telomeres are not folded when cells enter replicative senescence, which occurs independently of short telomere length. Indeed, Sir2, Sin3 and Set2 protein levels are decreased during senescence and their absence may thereby prevent telomere folding. Additionally, we show that the homologous recombination machinery, including the Rad51 and Rad52 proteins, as well as the checkpoint component Rad53 are essential for establishing the telomere fold-back structure. This study outlines a method to interrogate telomere-subtelomere interactions at a single unmodified yeast telomere. Using this method, we provide insights into how the spatial arrangement of the chromosome end structure is established and demonstrate that telomere folding is compromised throughout replicative senescence. Author summaryTelomeres are the protective caps of chromosome ends and prevent the activation of a local DNA damage response. In many organisms, telomeres engage in a loop-like structure which may provide an additional layer of end protection. As we still lack insight into the regulation of the folded telomere structure, we used budding yeast to establish a method to measure telomere folding and then study the genetic requirements for its establishment. We found that cells require the homologous recombination machinery as well as components of the DNA damage checkpoint to successfully establish a folded telomere. Through the deletion of telomerase in budding yeast, we investigated how telomere folding was regulated during replicative senescence, a process that occurs in the majority of telomerase negative human cells. During senescence, telomeres gradually shorten and erode until cells stop dividing which is a potent tumor suppressor and prevents unscheduled growth of potential cancer cells. We found, that the folded telomere structure is compromised as part of the cellular senescence response, but not due to telomere shortening per se. We think, that an altered telomeric chromatin environment during senescence is important to maintain an open state - which may be important for signaling or for repair.

genetics↗

bioRxiv2018

Functional impact of the H2A.Z histone variant during meiosis in Saccharomyces cerevisiae

Among the collection of chromatin modifications that influence its function and structure, the substitution of canonical histones by the so-called histone variants is one of the most prominent actions. Since crucial meiotic transactions are modulated by chromatin, here we investigate the functional contribution of the H2A.Z histone variant during both unperturbed meiosis and upon challenging conditions where the meiotic recombination checkpoint is triggered in budding yeast by the absence of the synaptonemal complex component Zip1. We have found that H2A.Z localizes to meiotic chromosomes in an SWR1-dependent manner. Although meiotic recombination is not substantially altered, the htz1 mutant (lacking H2A.Z) shows inefficient meiotic progression, impaired sporulation and reduced spore viability. These phenotypes are likely accounted for by the misregulation of meiotic gene expression landscape observed in htz1. In the zip1 mutant, the absence of H2A.Z results in a tighter meiotic arrest imposed by the meiotic recombination checkpoint. We have found that Mec1-dependent Hop1-T318 phosphorylation and the ensuing Mek1 activation are not significantly altered in zip1 htz1; however, downstream checkpoint targets, such as the meiosis I-promoting factors Ndt80, Cdc5 and Clb1, are drastically down-regulated. The study of the checkpoint response in zip1 htz1 has also allowed us to reveal the existence of an additional function of the Swe1 kinase, independent of CDK inhibitory phosphorylation, which is relevant to restrain meiotic cell cycle progression. In summary, our study shows that the H2A.Z histone variant impacts various aspects of meiotic development adding further insight into the relevance of chromatin dynamics for accurate gametogenesis.

genetics↗