Can current native tree seedling production and infrastructure meet an increasing forest restoration demand in Brazil?

Recent global commitments have placed forest and landscape restoration at the forefront of countries' efforts to recover ecosystem services, conserve biodiversity, and mitigate the effects of climate change. However, it needs to be asked if current native tree seedling supply meets an increase in demand for forest restoration? This study assessed the current configuration, distribution, and production capacity of forest nurseries producing native trees in Brazil. Brazil provides an interesting example of how global agreements aligned with national policies can lead to the proliferation of native seedling nurseries, and the challenges faced to restore species‐rich native forest ecosystems. We found that the nurseries in the Atlantic Forest region can still meet an increase in demand—both in terms of seedling quantity and diversity—because most of their production capacity is not currently used. However, not all Brazilian biomes have sufficient nurseries to meet restoration demands, thus there is a risk of using native species from a few biogeographical regions in a much spatially wider and ecologically diverse area. In addition, lack of seed supply and qualified labor can hamper the growth of the market. Barriers to seed supply may also lead to low levels of genetic variability and floristic representation in the populations and ecosystems to be restored. We conclude that restoration of high‐diversity forest ecosystems requires policies and supportive programs, with emphasis on private nurseries, to guarantee adequate supply of native tree seedlings and provide the necessary incentives to develop the emergent economy of forest restoration.     

Cell type discovery and representation in the era of high-content single cell phenotyping

Background

A fundamental characteristic of multicellular organisms is the specialization of functional cell types through the process of differentiation. These specialized cell types not only characterize the normal functioning of different organs and tissues, they can also be used as cellular biomarkers of a variety of different disease states and therapeutic/vaccine responses. In order to serve as a reference for cell type representation, the Cell Ontology has been developed to provide a standard nomenclature of defined cell types for comparative analysis and biomarker discovery. Historically, these cell types have been defined based on unique cellular shapes and structures, anatomic locations, and marker protein expression. However, we are now experiencing a revolution in cellular characterization resulting from the application of new high-throughput, high-content cytometry and sequencing technologies. The resulting explosion in the number of distinct cell types being identified is challenging the current paradigm for cell type definition in the Cell Ontology.

Results

In this paper, we provide examples of state-of-the-art cellular biomarker characterization using high-content cytometry and single cell RNA sequencing, and present strategies for standardized cell type representations based on the data outputs from these cutting-edge technologies, including “context annotations” in the form of standardized experiment metadata about the specimen source analyzed and marker genes that serve as the most useful features in machine learning-based cell type classification models. We also propose a statistical strategy for comparing new experiment data to these standardized cell type representations.

Conclusion

The advent of high-throughput/high-content single cell technologies is leading to an explosion in the number of distinct cell types being identified. It will be critical for the bioinformatics community to develop and adopt data standard conventions that will be compatible with these new technologies and support the data representation needs of the research community. The proposals enumerated here will serve as a useful starting point to address these challenges.

     

Probable advanced hydroid from the Early Ordovician of China

A fossil of a colonial organism with pyritized soft tissues of elongated fusiform zooids, found in the middle part of the early Floian Fenxiang Formation in Hubei Province of China, probably represents the oldest reliable record of a hydroid cnidarian. The preservation of the fossil is sufficiently different from that of associated carbonized skeletons of graptolites to exclude affinities with this group. The fossil is unlikely to be a bryozoan because of the mode of budding from proximal, not distal, parts of parent zooids, which is typical rather of hydroids. Although no thecae are preserved, the fossil, named Sinobryon elongatum gen. et sp. nov., is suggested to be a thecate hydroid, possibly related to the Haleciidae. The apparent presence of an advanced member of the thecaphoran Macrocolonia clade in strata 470 Ma old means that much of the hydroid (and cnidarian) diversification preceded the Middle Ordovician.     

Auricular Chromoblastomycosis: A Case Report and Review of Published Literature

Subcutaneous chromoblastomycosis is an infection commonly seen in tropical and subtropical climates, usually caused by trauma with vegetables and often affects the host’s lower limbs. We report a case of auricular chromoblastomycosis in a 67-year-old man and discuss the rarity of this clinical manifestation of chromoblastomycosis in the medical literature. In the present case, the etiologic agent was Fonsecaea pedrosoi, the most common agent found in Brazil.     

Requirement of UNC93B1 reveals a critical role for TLR7 in host resistance to primary infection with Trypanosoma cruzi

UNC93B1 associates with TLR3, 7, and 9, mediating their translocation from the endoplasmic reticulum to the endolysosome, thus allowing proper activation by microbial nucleic acids. We found that the triple-deficient 3d mice, which lack functional UNC93B1 as well as functional endosomal TLRs, are highly susceptible to infection with Trypanosoma cruzi. The enhanced parasitemia and mortality in 3d animals were associated with impaired proinflammatory response, including reduced levels of IL-12p40 and IFN-γ. Importantly, the phenotype of 3d mice was intermediary between MyD88(-/-) (highly susceptible) and TLR9(-/-) (moderately susceptible), indicating the involvement of an additional UN93B1-dependent TLR(s) on host resistance to T. cruzi. Hence, our experiments also revealed that TLR7 is a critical innate immune receptor involved in recognition of parasite RNA, induction of IL-12p40 by dendritic cells, and consequent IFN-γ by T lymphocytes. Furthermore, we show that upon T. cruzi infection, triple TLR3/7/9(-/-) mice had similar phenotype than 3d mice. These data imply that the nucleic acid-sensing TLRs are critical determinants of host resistance to primary infection with T. cruzi.     

Discovery of a novel family of CDK inhibitors with the program LIDAEUS: structural basis for ligand-induced disordering of the activation loop

A family of 4-heteroaryl-2-amino-pyrimidine CDK2 inhibitor lead compounds was discovered with the new database-mining program LIDAEUS through in silico screening. Four compounds with IC(50) values ranging from 17 to 0.9 microM were selected for X-ray crystal analysis. Two distinct binding modes are observed, one of which resembles the hydrogen bonding pattern of bound ATP. In the second binding mode, the ligands trigger a conformational change in the activation T loop by inducing movement of Lys(33) and Asp(145) side chains. The family of molecules discovered provides an excellent starting point for the design and synthesis of tight binding inhibitors, which may lead to a new class of antiproliferative drugs.     

Identification and characterization of the ‘missing’ terminal enzyme for siroheme biosynthesis in α‐proteobacteria

It has recently been shown that the biosynthetic route for both the d₁‐haem cofactor of dissimilatory cd₁ nitrite reductases and haem, via the novel alternative‐haem‐synthesis pathway, involves siroheme as an intermediate, which was previously thought to occur only as a cofactor in assimilatory sulphite/nitrite reductases. In many denitrifiers (which require d₁‐haem), the pathway to make siroheme remained to be identified. Here we identify and characterize a sirohydrochlorin–ferrochelatase from Paracoccus pantotrophus that catalyses the last step of siroheme synthesis. It is encoded by a gene annotated as cbiX that was previously assumed to be encoding a cobaltochelatase, acting on sirohydrochlorin. Expressing this chelatase from a plasmid restored the wild‐type phenotype of an Escherichia coli mutant‐strain lacking sirohydrochlorin–ferrochelatase activity, showing that this chelatase can act in the in vivo siroheme synthesis. A ΔcbiX mutant in P. denitrificans was unable to respire anaerobically on nitrate, proving the role of siroheme as a precursor to another cofactor. We report the 1.9 Å crystal structure of this ferrochelatase. In vivo analysis of single amino acid variants of this chelatase suggests that two histidines, His127 and His187, are essential for siroheme synthesis. This CbiX can generally be identified in α‐proteobacteria as the terminal enzyme of siroheme biosynthesis.     

Semaphorin 3F and Neuropilin-2 Control the Migration of Human T-Cell Precursors

Neuropilins and semaphorins are known as modulators of axon guidance, angiogenesis, and organogenesis in the developing nervous system, but have been recently evidenced as also playing a role in the immune system. Here we describe the expression and role of semaphorin 3F (SEMA3F) and its receptor neuropilin-2 (NRP2) in human T cell precursors. NRP2 and SEMA3F are expressed in the human thymus, in both lymphoid and non-lymphoid compartments. SEMA3F have a repulsive effect on thymocyte migration and inhibited CXCL12- and sphingosine-1-phosphate (S1P)-induced thymocyte migration by inhibiting cytoskeleton reorganization prior to stimuli. Moreover, NRP2 and SEMA3F are expressed in human T-cell acute lymphoblastic leukemia/lymphoma primary cells. In these tumor cells, SEMA3F also blocks their migration induced by CXCL12 and S1P. Our data show that SEMA3F and NRP2 are further regulators of human thymocyte migration in physiological and pathological conditions.