Laursencannon1726

Syndiniales are a ubiquitous group of protist parasites that infect and kill a wide range of hosts, including harmful bloom-forming dinoflagellates. Despite the importance of parasitism as an agent of plankton mortality, parasite-host dynamics remain poorly understood, especially over time, hindering the inclusion of parasitism in food web and ecosystem models. For a full year in the Skidaway River Estuary (Georgia), we employed weekly 18S rRNA sampling and co-occurrence network analysis to characterize temporal parasite-host infection dynamics of Syndiniales. Over the year, Syndiniales exhibited strong temporal variability, with higher relative abundance from June to October (7 to 28%) than other months in the year (0.01% to 6%). Nonmetric dimensional scaling of Syndiniales composition revealed tight clustering in June to October that coincided with elevated temperatures (23 to 31°C), though in general, abiotic factors poorly explained composition (canonical correspondence analysis [CCA] and partial least-sq web models.Salmonella enterica serovar Newport (S Newport) infections are gradually on the rise in China from the last decade. For humans' infections, S Newport has been ranked among the top five serovars responsible for persistent infections, globally. A total of 290 S. Newport strains with their relevant clinical metadata were analyzed, and the strains were subjected to whole-genome sequence analysis. Among these, 62.4% (n = 181) were from diarrheic patients and 28.9% (n = 84) were from asymptomatic individuals (including adults and youngsters) while 8.6% (n = 25) were from cases of persistent diarrhea in infants (28%, n = 7) and toddlers (72%, n = 18). The association between the sequence types (STs) and the variations in the clinical presentation was statistically significant (P = 0.0432), with ST46 causing diarrhea or representing asymptomatic patients and ST31 or ST68 causing persistent diarrhea. Genomic analysis revealed that the highest proportion of the isolates (98.5%, n = 279), primarily from patients with oron because of the presence of multiple acquired antimicrobial resistance determinants in such strains.In all cells, progression through the cell cycle occurs only when sufficient growth has occurred. Thus, cells must translate growth into a proportional signal that can be used to measure and transmit information about growth. Previous genetic studies in budding yeast suggested that related kinases called Gin4 and Hsl1 could function in mechanisms that measure bud growth; however, interpretation of the data was complicated by the use of gene deletions that cause complex terminal phenotypes. Here, we used the first conditional alleles of Gin4 and Hsl1 to more precisely define their functions. We show that excessive bud growth during a prolonged mitotic delay is an immediate consequence of inactivating Gin4 and Hsl1. Thus, acute loss of Gin4 and Hsl1 causes cells to behave as though they cannot detect that bud growth has occurred. We further show that Gin4 and Hsl1 undergo gradual hyperphosphorylation during bud growth that is dependent upon growth and correlated with the extent of growth. Moreover, gradual hyperphosphorylation of Gin4 during bud growth requires binding to anionic phospholipids that are delivered to the growing bud. While alternative models are possible, the data suggest that signaling lipids delivered to the growing bud generate a growth-dependent signal that could be used to measure bud growth.Small non-coding RNAs are central regulators of genome activity and stability. Their regulatory function typically involves sequence similarity with their target sites, but understanding the criteria by which they specifically recognize and regulate their targets across the genome remains a major challenge in the field, especially in the face of the diversity of silencing pathways involved. The dominance hierarchy among self-incompatibility alleles in Brassicaceae is controlled by interactions between a highly diversified set of small non-coding RNAs produced by dominant S-alleles and their corresponding target sites on recessive S-alleles. By controlled crosses, we created numerous heterozygous combinations of S-alleles in Arabidopsis halleri and developed an RT-qPCR assay to compare allele-specific transcript levels for the pollen determinant of self-incompatibility (SCR). This provides the unique opportunity to evaluate the precise base-pairing requirements for effective transcriptional regulation of this target gene. We found strong transcriptional silencing of recessive SCR alleles in all heterozygote combinations examined. A simple threshold model of base-pairing for the sRNA-target interaction captures most of the variation in SCR transcript levels. For a subset of S-alleles, we also measured allele-specific transcript levels of the determinant of pistil specificity (SRK) and found sharply distinct expression dynamics throughout flower development between SCR and SRK In contrast to SCR, both SRK alleles were expressed at similar levels in the heterozygote genotypes examined, suggesting no transcriptional control of dominance for this gene. selleck chemicals We discuss the implications for the evolutionary processes associated with the origin and maintenance of the dominance hierarchy among self-incompatibility alleles.Bacteria often carry "extra DNA" in form of plasmids in addition to their chromosome. Many plasmids have a copy number greater than one such that the genes encoded on these plasmids are present in multiple copies per cell. This has evolutionary consequences by increasing the mutational target size, by prompting the (transitory) co-occurrence of mutant and wild-type alleles within the same cell, and by allowing for gene dosage effects. We develop and analyze a mathematical model for bacterial adaptation to harsh environmental change if adaptation is driven by beneficial alleles on multicopy plasmids. Successful adaptation depends on the availability of advantageous alleles and on their establishment probability. The establishment process involves the segregation of mutant and wild-type plasmids to the two daughter cells, allowing for the emergence of mutant-homozygous cells over the course of several generations. To model this process, we use the theory of multi-type branching processes, where a type is defined by the genetic composition of the cell.