Conserving species' evolutionary potential and history: Opportunities under the Kunming–Montreal Global Biodiversity Framework

Genetic diversity (GD) and phylogenetic diversity (PD) respectively represent species' evolutionary potential and history, and support most of the biodiversity benefits to humanity. Yet, these two biodiversity facets have been overlooked in previous biodiversity policies. As the Parties to the Convention on Biological Diversity (CBD) adopted the Kunming–Montreal Global Biodiversity Framework (GBF) in December 2022, we analyze how GD and PD are considered in this new framework and discuss how their incorporation in the GBF could strengthen their conservation. Although the inclusion of certain indicators could be elevated, both GD and PD are an integral part of the recently adopted GBF. This represents a significant improvement compared to the CBD strategic plan 2011–2020 and an unprecedented opportunity to bring species' evolutionary potential and history to the core of public biodiversity policies. We urge the scientific community to leverage this opportunity to actually improve the conservation of species' evolutionary potential and history

A comparison of deformed wing virus in deformed and asymptomatic honey bees

Deformed wing virus (DWV) in association with Varroa destructor is currently attributed to being responsible for colony collapse in the western honey bee (Apis mellifera). The appearance of deformed individuals within an infested colony has long been associated with colony losses. However, it is unknown why only a fraction of DWV positive bees develop deformed wings. This study concerns two small studies comparing deformed and non-deformed bees. In Brazil, asymptomatic bees (no wing deformity) that had been parasitised by Varroa as pupae had higher DWV loads than non-parasitised bees. However, we found no greater bilateral asymmetry in wing morphology due to DWV titres or parasitisation. As expected, using RT-qPCR, deformed bees were found to contain the highest viral loads. In a separate study, next generation sequencing (NGS) was applied to compare the entire DWV genomes from paired symptomatic and asymptomatic bees from three colonies on two different Hawaiian islands. This revealed no consistent differences between DWV genomes from deformed or asymptomatic bees, with the greatest variation seen between locations, not phenotypes. All samples, except one, were dominated by DWV type A. This small-scale study suggests that there is no unique genetic variant associated with wing deformity; but that many DWV variants have the potential to cause deformit

Peripheral nervous system plasmalogens regulate Schwann cell differentiation and myelination

Rhizomelic chondrodysplasia punctata (RCDP) is a developmental disorder characterized by hypotonia, cataracts, abnormal ossification, impaired motor development, and intellectual disability. The underlying etiology of RCDP is a deficiency in the biosynthesis of ether phospholipids, of which plasmalogens are the most abundant form in nervous tissue and myelin; however, the role of plasmalogens in the peripheral nervous system is poorly defined. Here, we used mouse models of RCDP and analyzed the consequence of plasmalogen deficiency in peripheral nerves. We determined that plasmalogens are crucial for Schwann cell development and differentiation and that plasmalogen defects impaired radial sorting, myelination, and myelin structure. Plasmalogen insufficiency resulted in defective protein kinase B (AKT) phosphorylation and subsequent signaling, causing overt activation of glycogen synthase kinase 3β (GSK3β) in nerves of mutant mice. Treatment with GSK3β inhibitors, lithium, or 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8) restored Schwann cell defects, effectively bypassing plasmalogen deficiency. Our results demonstrate the requirement of plasmalogens for the correct and timely differentiation of Schwann cells and for the process of myelination. In addition, these studies identify a mechanism by which the lack of a membrane phospholipid causes neuropathology, implicating plasmalogens as regulators of membrane and cell signaling.We thank Paula Sampaio for microscopy support, Paula Magalhdes for genotyping, and Isabel Carvalho, Sofia Lamas, and Fatima Martins for excellent animal care. We are grateful to P. Brophy (University of Edinburgh) for the DRP2 antibody and to M. Baes (K.U. Leuven) for providing the Gnpat mouse strain. This work was funded by the Research Foundation of the European Leukodystrophy Association (ELA 2008-009C4, ELA 2010-042C5), by FEDER Funds through the Operational Competitiveness Program - COMPETE, and by national funds through the FCT - Fundacao para a Ciencia e a Tecnologia under the project FCOMP-01-0124-FEDER-015970 (PTDS/SAU-ORG/112406/2009). P. Brites is an FCT Investigator, and T. Ferreira da Silva was supported by the FCT (SFRH/BD/88160/2012)

Analisando a aplicação de um Bingo Químico sobre tabela periódica: uma experiência no Ensino Médio a partir do PIBID/UNIR

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Genome of the Avirulent Human-Infective Trypanosome—Trypanosoma rangeli

Background: Trypanosoma rangeli is a hemoflagellate protozoan parasite infecting humans and other wild and domestic mammals across Central and South America. It does not cause human disease, but it can be mistaken for the etiologic agent of Chagas disease, Trypanosoma cruzi. We have sequenced the T. rangeli genome to provide new tools for elucidating the distinct and intriguing biology of this species and the key pathways related to interaction with its arthropod and mammalian hosts.  Methodology/Principal Findings: The T. rangeli haploid genome is ,24 Mb in length, and is the smallest and least repetitive trypanosomatid genome sequenced thus far. This parasite genome has shorter subtelomeric sequences compared to those of T. cruzi and T. brucei; displays intraspecific karyotype variability and lacks minichromosomes. Of the predicted 7,613 protein coding sequences, functional annotations could be determined for 2,415, while 5,043 are hypothetical proteins, some with evidence of protein expression. 7,101 genes (93%) are shared with other trypanosomatids that infect humans. An ortholog of the dcl2 gene involved in the T. brucei RNAi pathway was found in T. rangeli, but the RNAi machinery is non-functional since the other genes in this pathway are pseudogenized. T. rangeli is highly susceptible to oxidative stress, a phenotype that may be explained by a smaller number of anti-oxidant defense enzymes and heatshock proteins.  Conclusions/Significance: Phylogenetic comparison of nuclear and mitochondrial genes indicates that T. rangeli and T. cruzi are equidistant from T. brucei. In addition to revealing new aspects of trypanosome co-evolution within the vertebrate and invertebrate hosts, comparative genomic analysis with pathogenic trypanosomatids provides valuable new information that can be further explored with the aim of developing better diagnostic tools and/or therapeutic targets

Nppa and Nppb act redundantly during zebrafish cardiac development to confine AVC marker expression and reduce cardiac jelly volume

() and () form a gene cluster with expression in the chambers of the developing heart. Despite restricted expression, a function in cardiac development has not been demonstrated by mutant analysis. This is attributed to functional redundancy however their genomic location has impeded formal analysis. Using genome-editing, we generated mutants for and and found single mutants indistinguishable from wildtype whereas / double mutants display heart morphogenesis defects and pericardial oedema. Analysis of atrioventricular canal (AVC) markers show expansion of , and expression into the atrium of double mutants. This expanded expression correlates with increased extracellular matrix in the atrium. Using a biosensor for Hyaluronic acid to measure the cardiac jelly (cardiac extracellular matrix), we confirm cardiac jelly expansion in / double mutants. Finally, knockdown rescues the expansion of expression and cardiac jelly in double mutants. This definitively shows that and function redundantly during cardiac development to restrict gene expression to the AVC, preventing excessive cardiac jelly synthesis in the atrial chamber

Guideline Materials and Documentation for the Genetic Diversity Indicators of the Monitoring Framework for the Kunming-Montreal Global Biodiversity Framework

Genetic diversity is fundamental to biological diversity, vital for species’ health and adaptation to environmental change. Under the recently adopted Kunming-Montreal Global Biodiversity Framework (GBF), 196 Parties committed to report the status of genetic diversity for both wild and domesticated species. For this, three genetic diversity indicators were developed, two of which focus on processes contributing to genetic diversity conservation: ensuring that populations are large enough to maintain genetic diversity (effective population size Ne 500 indicator) and maintaining genetically distinct populations (populations maintained, PM indicator). A third indicator focuses on the number of species being monitored using DNA-based methods. Adopted by 196 CBD Parties in December 2022, GBF integrated Ne 500 and PM as headline and complementary indicators, respectively. To aid nations in quantifying these indicators, a detailed set of guideline materials was developed, encompassing species selection, data compilation, and indicator computation. These guidelines draw from the collaborative efforts of the first multinational assessment of genetic diversity indicators that was recently completed and that will be refined continually through a versioning system, as more experience is gained and shared. The materials aim to support the global monitoring framework established by the CBD and are accessible online for utilization and updates. The guidelines are available at this link.