The Erwin equation of biodiversity: From little steps to quantum leaps in the discovery of tropical insect diversity

Almost 40 years ago, Terry L. Erwin published a seemingly audacious proposition: There may be as many as 30 million species of insects in the world. Here, we translate Erwin's verbal argument into a diversity-ratio model—the Erwin Equation of Biodiversity—and discuss how it has inspired other biodiversity estimates. We categorize, describe the assumptions for, and summarize the most commonly used methods for calculating estimates of global biodiversity. Subsequent diversity-ratio extrapolations have incorporated parameters representing empirical insect specialization ratios, and how insect specialization changes at different spatial scales. Other approaches include macroecological diversity models and diversity curves. For many insect groups with poorly known taxonomies, diversity estimates are based on the opinions of taxonomic experts. We illustrate our current understanding of insect diversity by focusing on the six most speciose insect orders worldwide. For each order, we compiled estimates of the (a) maximum estimated number of species, (b) minimum estimated number of species, and (c) number of currently described species. By integrating these approaches and considering new information, we believe an estimate of 5.5 million species of insects in the world is much too low. New molecular methodologies (e.g., metabarcoding and NGS studies) are revealing daunting numbers of cryptic and previously undescribed species, at the same time increasing our precision but also uncertainty about present estimates. Not until technologies advance and sampling become more comprehensive, especially of tropical biotas, will we be able to make robust estimates of the total number of insect species on Earth.     

Divergent roles of HDAC1 and HDAC2 in the regulation of epidermal development and tumorigenesis

The histone deacetylases HDAC1 and HDAC2 remove acetyl moieties from lysine residues of histones and other proteins and are important regulators of gene expression. By deleting different combinations of Hdac1 and Hdac2 alleles in the epidermis, we reveal a dosage‐dependent effect of HDAC1/HDAC2 activity on epidermal proliferation and differentiation. Conditional ablation of either HDAC1 or HDAC2 in the epidermis leads to no obvious phenotype due to compensation by the upregulated paralogue. Strikingly, deletion of a single Hdac2 allele in HDAC1 knockout mice results in severe epidermal defects, including alopecia, hyperkeratosis, hyperproliferation and spontaneous tumour formation. These mice display impaired Sin3A co‐repressor complex function, increased levels of c‐Myc protein, p53 expression and apoptosis in hair follicles (HFs) and misregulation of HF bulge stem cells. Surprisingly, ablation of HDAC1 but not HDAC2 in a skin tumour model leads to accelerated tumour development. Our data reveal a crucial function of HDAC1/HDAC2 in the control of lineage specificity and a novel role of HDAC1 as a tumour suppressor in the epidermis.     

Water Scarcity in the Andes: A Comparison of Local Perceptions and Observed Climate, Land Use and Socioeconomic Changes

In the Andean region of South America, understanding communities’ water perceptions is particularly important for water management as many rural communities must decide by themselves if and how they will protect their micro-watersheds and distribute their water. In this study we examine how Water User Associations in the Eastern Andes of Colombia perceive water scarcity and the relationship between this perception and observed climate, land use, and demographic changes. Results demonstrate a complex relationship between perceptions and observed changes. On the one hand, observed changes in land cover match perceptions of deforestation as the primary cause of increasing water scarcity. On the other hand, perceptions of climate driven changes in water availability are not reflected in observed precipitation data. Furthermore, water scarcity was perceived in regions where seasonal rainfall variability is higher but not in regions where annual rainfall is lower. We discuss how these results contribute to our understanding of adaptation to climate change and the implications of possible mismatches between environmental changes and local perceptions.     

The Solution Structure of a Locked Nucleic Acid (LNA) Hybridized to DNA

Abstract

LNA (Locked Nucleic Acids) is a novel oligonucleotide analogue containing a conformationally restricted nucleotide with a 2′-0, 4′-C-methylene bridge that induces unprecedented thermal affinities when mixed with complementary single stranded DNA and RNA. We have used two-dimensional'H NMR spectroscopy obtained at 750 and 500 MHz to determine a high resolution solution structure of an LNA oligonucleotide hybridized to the complementary DNA strand. The determination of the structure was based on a complete relaxation matrix analysis of the NOESY cross peaks followed by restrained molecular dynamics calculations. Forty final structures were generated for the duplex from A-type and B-type dsDNA starting structures. The root-mean-square deviation (RMSD) of the coordinates for the forty structures of the complex was 0.32Å. The structures were analysed by use of calculated helix parameters. This showed that the values for rise and buckle in the LNA duplex is markedly different from canonical B-DNA at the modification site. A value of twist similar to A-DNA is also observed at the modification site. The overall length of the helix which is 27.3Å. The average twist over the sequence are 35.9° ± 0.3°. Consequently, the modification does not cause the helix to unwind. The bis-intercalation of the thiazole orange dye TOTO to the LNA duplex was also investigated by ¹H NMR spectroscopy to sense the structural change from the unmodified oligonucleotide. We observed that the bis-intercalation of TOTO is much less favourable in the 5′-CT^LAG-3′ site than in the unmodified 5′-CT^LAG-3′ site. This was related to the change in the base stacking of the LNA duplex compared to the unmodified duplex.     

Host mTORC1 Signaling Regulates Andes Virus Replication

Hantavirus pulmonary syndrome (HPS) is a severe respiratory disease characterized by pulmonary edema, with fatality rates of 35 to 45%. Disease occurs following infection with pathogenic New World hantaviruses, such as Andes virus (ANDV), which targets lung microvascular endothelial cells. During replication, the virus scavenges 5′-m⁷G caps from cellular mRNA to ensure efficient translation of viral proteins by the host cell cap-dependent translation machinery. In cells, the mammalian target of rapamycin (mTOR) regulates the activity of host cap-dependent translation by integrating amino acid, energy, and oxygen availability signals. Since there is no approved pharmacological treatment for HPS, we investigated whether inhibitors of the mTOR pathway could reduce hantavirus infection. Here, we demonstrate that treatment with the FDA-approved rapamycin analogue temsirolimus (CCI-779) blocks ANDV protein expression and virion release but not entry into primary human microvascular endothelial cells. This effect was specific to viral proteins, as temsirolimus treatment did not block host protein synthesis. We confirmed that temsirolimus targeted host mTOR complex 1 (mTORC1) and not a viral protein, as knockdown of mTORC1 and mTORC1 activators but not mTOR complex 2 components reduced ANDV replication. Additionally, primary fibroblasts from a patient with tuberous sclerosis exhibited increased mTORC1 activity and increased ANDV protein expression, which were blocked following temsirolimus treatment. Finally, we show that ANDV glycoprotein Gn colocalized with mTOR and lysosomes in infected cells. Together, these data demonstrate that mTORC1 signaling regulates ANDV replication and suggest that the hantavirus Gn protein may modulate mTOR and lysosomal signaling during infection, thus bypassing the cellular regulation of translation.     

Tradeoffs in basal area growth and reproduction shift over the lifetime of a long-lived tropical species

Understanding of the extent to which reproductive costs drive growth largely derives from reproductively mature temperate trees in masting and non-masting years. We modeled basal area increment (BAI) and explored current growth–reproduction tradeoffs and changes in such allocation over the life span of a long-lived, non-masting tropical tree. We integrated rainfall and soil variables with data from 190 Bertholletia excelsa trees of different diameter at breast height (DBH) sizes, crown characteristics, and liana loads, quantifying BAI and reproductive output over 4 and 6 years, respectively. While rainfall explains BAI in all models, regardless of DBH class or ontogenic stage, light (based on canopy position and crown form) is most critical in the juvenile (5 cm ≤ DBH < 50 cm) phase. Suppressed trees are only present as juveniles and grow ten times slower (1.45 ± 2.73 m² year^?1) than trees in dominant and co-dominant positions (13.25 ± 0.82 and 12.90 ± 1.35 m² year^?1, respectively). Additionally, few juvenile trees are reproductive, and those that are, demonstrate reduced growth, as do reproductive trees in the next 50 to 100 cm DBH class, suggesting growth–reproduction tradeoffs. Upon reaching the canopy, however, and attaining a sizeable girth, this pattern gradually shifts to one where BAI and reproduction are influenced independently by variables such as liana load, crown size and soil properties. At this stage, BAI is largely unaffected by fruit production levels. Thus, while growth–reproduction tradeoffs clearly exist during early life stages, effects of reproductive allocation diminish as B. excelsa increases in size and maturity.