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Forecasting the spatiotemporal spread of infectious diseases during an outbreak is an important component of epidemic response. However, it remains challenging both methodologically and with respect to data requirements, as disease spread is influenced by numerous factors, including the pathogen’s underlying transmission parameters and epidemiological dynamics, social networks and population connectivity, and environmental conditions. Here, using data from Sierra Leone, we analyze the spatiotemporal dynamics of recent cholera and Ebola outbreaks and compare and contrast the spread of these two pathogens in the same population. We develop a simulation model of the spatial spread of an epidemic in order to examine the impact of a pathogen’s incubation period on the dynamics of spread and the predictability of outbreaks. We find that differences in the incubation period alone can determine the limits of predictability for diseases with different natural history, both empirically and in our simulations. Our results show that diseases with longer incubation periods, such as Ebola, where infected individuals can travel farther before becoming infectious, result in more long-distance sparking events and less predictable disease trajectories, as compared to the more predictable wave-like spread of diseases with shorter incubation periods, such as cholera.Voiced sound production is the primary form of acoustic communication in terrestrial vertebrates, particularly birds and mammals, including humans. Developing a causal physics-based model that ultimately links descending vocal motor control to tissue vibration and sound requires embodied approaches that include realistic representations of voice physiology. Here, we first implement and then experimentally test a high-fidelity three-dimensional (3D) continuum model for voiced sound production in birds. Driven by individual-based physiologically quantifiable inputs, combined with noninvasive inverse methods for tissue material parameterization, our model accurately predicts observed key vibratory and acoustic performance traits. These results demonstrate that realistic models lead to accurate predictions and support the continuum model approach as a critical tool toward a causal model of voiced sound production.Bacillus anthracis, the etiological agent of anthrax, is a well-established model organism. For B. anthracis and most other infectious diseases, knowledge regarding transmission and infection parameters in natural systems, in large part, comprises data gathered from closely controlled laboratory experiments. Fatal, natural anthrax infections transmit the bacterium through new host-pathogen contacts at carcass sites, which can occur years after death of the previous host. For the period between contact and death, all of our knowledge is based upon experimental data from domestic livestock and laboratory animals. Here we use a noninvasive method to explore the dynamics of anthrax infections, by evaluating the terminal diversity of B. anthracis in anthrax carcasses. We present an application of population genetics theory, specifically, coalescence modeling, to intrainfection populations of B. anthracis to derive estimates for the duration of the acute phase of the infection and effective population size converted to the number of colony-forming units establishing infection in wild plains zebra (Equus quagga). Founding populations are small, a few colony-forming units, and infections are rapid, lasting roughly between 1 d and 3 d in the wild. Our results closely reflect experimental data, showing that small founding populations progress acutely, killing the host within days. We believe this method is amendable to other bacterial diseases from wild, domestic, and human systems. Copyright © 2020 the Author(s). Published by PNAS.jing he sheng1 (jhs1) is a mutant of the DNA2 homolog in Arabidopsis (Arabidopsis thaliana), which was previously identified as being involved in DNA damage repair, cell cycle regulation, and meristem maintenance. A mutation at the 3′ intron splicing site of the 11th intron causes alternative splicing of this intron at two other sites, which results in frame shifts and premature stop codons. AZD0530 Here, we screened suppressors of jhs1 to further study the function and regulatory networks of JHS1. Three suppressors with wild type-like phenotypes were obtained. Sequencing analysis results showed that each of the suppressors has a second mutation in jhs1 that causes further alternative splicing of the intron and corrects the shifted reading frame with small insertions. Pre-mRNA sequence analysis and intron splicing site evaluation results suggested that intron splicing was disturbed in the suppressors, and this switched the splicing site, resulting in small insertions in the coding regions of JHS1. Structural analysis of JHS1 suggested that the insertions are in a disordered loop region of the DNA2 domain and do not seem to have much deleterious effect on the function of the protein. This work not only has implications for the evolution of protein sequences at exon junctions but also provides a strategy to study the mechanism of pre-mRNA splicing. copyright, serif 2020 American Society of Plant Biologists. All rights reserved.Plant receptor-like kinases (RLKs) control the initiation, development and maintenance of symbioses with beneficial mycorrhizal fungi and nitrogen-fixing bacteria. Carbohydrate perception activates symbiosis signalling via Lysin-motif (LysM) RLKs and subsequently the common symbiosis signalling pathway. As the receptors activated are often also immune receptors in multiple species, exactly how carbohydrate identities avoid immune activation and drive symbiotic outcome is still not fully understood. This may involve the coincident detection of additional signalling molecules that provide specificity. Because of the metabolic costs of supporting symbionts, the level of symbiosis development is fine-tuned by a range of local and mobile signals that are activated by various RLKs. Beyond early, pre-contact symbiotic signalling, signal exchanges ensue throughout infection, nutrient exchange and turnover of symbiosis. Here, we review the latest understanding on plant symbiosis signalling from the perspective of RLK-mediated pathways.