Effect of Hydrogen Bond Interaction on the Decomposition Temperature, Aromaticity, and Bond Order of Nonmetallic Pentazolate Salts

Nonmetallic pentazolate (cyclo-N5–) salts are novel polynitrogen high-energy-density materials with great potential and application prospects. Hydrogen bond networks play a vital role in improving the thermal stability of these compounds. In order to further increase the decomposition temperature (Td) and attain a more thorough exploration of these compounds, we evaluated and visualized the energy of hydrogen bonds (E_HBs) and the effects of HBs on Td, aromaticity, and the Mayer bond order (MBO). The increase in the total E_HBs can increase the Td, such as with 3,6,7-triamino-7H-[1,2,4]­triazolo­[4,3-b]­[1,2,4]­triazol-2-ium and biguanidinium pentazolates. Moreover, an increase in the maximum E_HBs can reduce the aromaticity of the cyclo-N5– anion and increase the difference between the maximum and minimum MBO, like 3,9-diamino-6,7-dihydro-5H-bis­([1,2,4]­triazolo)­[4,3-e:3′,4′-g]­[1,2,4,5]­tetrazepine-2,10- diium and O-(carboxymethyl)­hydroxylammonium pentazolates. In addition, increasing the number of donors of hydrogen bonds, especially the proportion of O–H bonds, can significantly increase the Td of pentazolate salts

Impaired peroxisomal import in Drosophila oenocytes causes cardiac dysfunction by inducing upd3 as a peroxikine

Aging is characterized by a chronic, low-grade inflammation, which is a major risk factor for cardiovascular diseases. It remains poorly understood whether pro-inflammatory factors released from non-cardiac tissues contribute to the non-autonomous regulation of age-related cardiac dysfunction. Here, we report that age-dependent induction of cytokine unpaired 3 (upd3) in Drosophila oenocytes (hepatocyte-like cells) is the primary non-autonomous mechanism for cardiac aging. We show that upd3 is significantly up-regulated in aged oenocytes. Oenocyte-specific knockdown of upd3 is sufficient to block aging-induced cardiac arrhythmia. We further show that the age-dependent induction of upd3 is triggered by impaired peroxisomal import and elevated JNK signaling in aged oenocytes. We term hormonal factors induced by peroxisome dysfunction as peroxikines. Intriguingly, oenocyte-specific overexpression of Pex5, the key peroxisomal import receptor, blocks age-related upd3 induction and alleviates cardiac arrhythmicity. Thus, our studies identify an important role of hepatocyte-specific peroxisomal import in mediating non-autonomous regulation of cardiac aging.This article is published as Huang, K., Miao, T., Chang, K. et al. Impaired peroxisomal import in Drosophila oenocytes causes cardiac dysfunction by inducing upd3 as a peroxikine. Nat Commun 11, 2943 (2020). https://doi.org/10.1038/s41467-020-16781-w. Posted with permission. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

Impaired peroxisomal import in Drosophila oenocytes causes cardiac dysfunction by inducing upd3 as a peroxikine

Aging is the major risk factor for cardiovascular diseases due to chronic, low-grade inflammation stemmed from pro-inflammatory factors circulating in the body. Here, the authors identify a role of hepatocyte specific peroxisomal import in mediating non-autonomous regulation of cardiac aging, through upregulation of IL6-like inflammatory cytokine

The SARS-CoV-2 Subgenome Landscape and its Novel Regulatory Features

International audienceCOVID-19, caused by Coronavirus SARS-CoV-2, is now in global pandemic. Coronaviruses are known to generate negative subgenomes through Transcription-Regulating Sequence (TRS)-dependent template switch, but the global dynamic landscapes of coronaviral subgenomes and regulatory rules remain unclear. Here, using NGS short-read and Nanopore long-read sequencing to profile poly(A) RNAs in two cell types at multiple time points post-infection of SARS-CoV-2, we identified hundreds of template switches and constructed the dynamic landscapes of SARS-CoV-2 subgenomes. Interestingly, template switch could occur in bidirectional manner, with diverse SARS-CoV-2 subgenomes generated from successive template switching events. Majority of template switches result from RNA-RNA interactions, including seed and compensatory modes, with terminal pairing status as a key determinant. Moreover, two TRS-independent template switch modes are also responsible for subgenome biogenesis. Collectively, our findings reveal the subgenome landscape of SARS-CoV-2 and its regulatory features, providing a molecular basis for the organization and regulation of coronaviral subgenomes

De novo assembly, annotation, and comparative analysis of 26 diverse maize genomes.

We report de novo genome assemblies, transcriptomes, annotations, and methylomes for the 26 inbreds that serve as the founders for the maize nested association mapping population. The number of pan-genes in these diverse genomes exceeds 103,000, with approximately a third found across all genotypes. The results demonstrate that the ancient tetraploid character of maize continues to degrade by fractionation to the present day. Excellent contiguity over repeat arrays and complete annotation of centromeres revealed additional variation in major cytological landmarks. We show that combining structural variation with single-nucleotide polymorphisms can improve the power of quantitative mapping studies. We also document variation at the level of DNA methylation and demonstrate that unmethylated regions are enriched for cis-regulatory elements that contribute to phenotypic variation