Crowdergentry8314

Shoot-borne adventitious/crown roots form a highly derived fibrous root system in grasses. The molecular mechanisms controlling their development remain largely unknown. selleck chemical Here, we provide a genome-wide landscape of transcriptional signatures - tightly regulated auxin response and in-depth spatio-temporal expression patterns of potential epigenetic modifiers - and transcription factors during priming and outgrowth of rice (Oryza sativa) crown root primordia. Functional analyses of rice transcription factors from WUSCHEL-RELATED HOMEOBOX and PLETHORA gene families reveal their non-redundant and species-specific roles in determining the root architecture. WOX10 and PLT1 regulate both shoot-borne crown roots and root-borne lateral roots, but PLT2 specifically controls lateral root development. PLT1 activates local auxin biosynthesis genes to promote crown root development. Interestingly, O. sativa PLT genes rescue lateral root primordia outgrowth defects of Arabidopsis plt mutants, demonstrating their conserved role in root primordia outgrowth irrespective of their developmental origin. Together, our findings unveil a molecular framework of tissue transdifferentiation during root primordia establishment, leading to the culmination of robust fibrous root architecture. This also suggests that conserved factors have evolved their transcription regulation to acquire species-specific function.

Blood eosinophil (EOS) counts and EOS cationic protein (ECP) levels associate positively with major cardiovascular disease (CVD) risk factors and prevalence. This study investigates the role of EOS in cardiac hypertrophy.

A retrospective cross-section study of 644 consecutive inpatients with hypertension examined the association between blood EOS counts and cardiac hypertrophy. Pressure overload- and β-adrenoreceptor agonist isoproterenol-induced cardiac hypertrophy was produced in EOS-deficient ΔdblGATA mice. This study revealed positive correlations between blood EOS counts and left ventricular (LV) mass and mass index in humans. ΔdblGATA mice showed exacerbated cardiac hypertrophy and dysfunction, with increased LV wall thickness, reduced LV internal diameter, and increased myocardial cell size, death, and fibrosis. Repopulation of EOS from wild-type mice, but not those from IL4-deficient mice ameliorated cardiac hypertrophy and cardiac dysfunctions. In ΔdblGATA and wild-type mice, administration of EOnic proteins in this human CVD.Zebrafish embryos are widely used for drug discovery, however, administering drugs to adult zebrafish is limited by current protocols that can cause stress. Here, we developed a drug formulation and administration method for adult zebrafish by producing food-based drug pellets that are consumed voluntarily. We applied this to zebrafish with BRAF-mutant melanoma, a model that has significantly advanced our understanding of melanoma progression, but not of drug resistance due to the limitations of current treatment methods. Zebrafish with melanomas responded to short-term, precise and daily dosing with drug pellets made with the BRAFV600E inhibitor, vemurafenib. On-target drug efficacy was determined by phospho-Erk staining. Continued drug treatment led to the emergence, for the first time in zebrafish, of acquired drug resistance and melanoma relapse, modelling the responses seen in melanoma patients. This method presents a controlled, non-invasive approach that permits long-term drug studies and can be widely applied to adult zebrafish models.Although a large number of mouse models have been made to study Alzheimer's disease, only a handful allow experimental control over the location or timing of the protein being used to drive pathology. Other fields have used the Cre and the tamoxifen-inducible CreER driver lines to achieve precise spatial and temporal control over gene deletion and transgene expression, yet these tools have not been widely used in studies of neurodegeneration. Here, we describe two strategies for harnessing the wide range of Cre and CreER driver lines to control expression of disease-associated amyloid precursor protein (APP) in modeling Alzheimer's amyloid pathology. We show that CreER-based spatial and temporal control over APP expression can be achieved with existing lines by combining a Cre driver with a tetracycline-transactivator (tTA)-dependent APP responder using a Cre-to-tTA converter line. We then describe a new mouse line that places APP expression under direct control of Cre recombinase using an intervening lox-stop-lox cassette. Mating this allele with a CreER driver allows both spatial and temporal control over APP expression, and with it, amyloid onset. This article has an associated First Person interview with the first author of the paper.The best-known plant endophytes include mainly fungi and bacteria, but there are also a few records of microalgae growing endophytically in vascular land plants, some of which belong to the genus Coccomyxa. In this study, we isolated a single-celled photosynthetic microorganism from the arsenic-tolerant shrub Acacia farnesiana, thus we hypothesized that it is an endophytic arsenic-tolerant microalga. The microorganism was identified as belonging to the genus Coccomyxa, and the observation of algal cells within the root tissues strongly suggests its endophytic nature. The alga's tolerance to arsenate (AsV) and its influence on the fitness of A. farnesiana in the presence of AsV were evaluated. Coccomyxa sp. can tolerate up to 2000 µM of AsV for periods shorter than 10 days, however, AsV-tolerance decreased significantly in longer exposure periods. The association with the microalga increased the pigment content in aboveground tissues of A. farnesiana seedlings exposed to AsV for 50 days, without changes in plant growth or arsenic accumulation. This work describes the association, probably endophytic, between an angiosperm and a microalga, confirming the ability of the genus Coccomyxa to form associations with land plants and broadening the known variety of plant endophytes.

The objective of the present study was to examine the effect of venovenous (VV) extracorporeal membrane oxygenation (ECMO) use on the haemodynamics during single lung transplantation (SLT) and postoperative course.

Forty-seven patients who underwent SLT for end-stage lung diseases in our lung transplant centre between January 2010 and December 2019 were included in this study. The recipients were divided into 3 groups according to the type of intraoperative ECMO. No type of ECMO was intra-operatively used in the patients of the no use of ECMO (NO ECMO) group. The patients in the venoarterial (VA) and VV ECMO groups were put on VA and VV ECMO during the surgery, respectively. The data were compared among the 3 groups.

There were 13 SLT cases in the NO ECMO group, 23 SLT cases in the VA ECMO group and 11 SLT cases in the VV ECMO group. Re-exploration for bleeding was performed in 3 (13.0%) recipients in the VA ECMO group. No recipients required re-exploration in the other groups. In the NO ECMO group, systolic pulmonary arterial pressure (PAP) was significantly elevated during the main pulmonary artery clamp on the SLT side and it was decreased in the VA ECMO group because of the bypass flow. Interestingly, systolic PAP was significantly decreased in the VV ECMO group as well.

VV ECMO decreases the PAP during SLT, which could be a choice for extracorporeal life support during lung transplant surgery for patients, even those with pulmonary hypertension.

VV ECMO decreases the PAP during SLT, which could be a choice for extracorporeal life support during lung transplant surgery for patients, even those with pulmonary hypertension.Gene drives are engineered alleles that can bias inheritance in their favor, allowing them to spread throughout a population. They could potentially be used to modify or suppress pest populations, such as mosquitoes that spread diseases. CRISPR/Cas9 homing drives, which copy themselves by homology-directed repair in drive/wild-type heterozygotes, are a powerful form of gene drive, but they are vulnerable to resistance alleles that preserve the function of their target gene. Such resistance alleles can prevent successful population suppression. Here, we constructed a homing suppression drive in Drosophila melanogaster that utilized multiplexed gRNAs to inhibit the formation of functional resistance alleles in its female fertility target gene. The selected gRNA target sites were close together, preventing reduction in drive conversion efficiency. The construct reached a moderate equilibrium frequency in cage populations without apparent formation of resistance alleles. However, a moderate fitness cost prevented elimination of the cage population, showing the importance of using highly efficient drives in a suppression strategy, even if resistance can be addressed. Nevertheless, our results experimentally demonstrate the viability of the multiplexed gRNAs strategy in homing suppression gene drives.Plants perceive a multitude of environmental signals and stresses, and integrate their response to them in ways that culminate in modified phenotypes, optimized for plant survival. This ability of plants, known as phenotypic plasticity, is found throughout evolution, in all plant lineages. For any given environment, the specifics of the response to a particular signal may vary depending on the plants' unique physiology and ecological niche. The bryophyte lineage, including mosses, which diverged from the vascular plants ~450-430 million years ago, represent a unique ecological and phylogenetic group in plant evolution. Several aspects of the moss life cycle, their morphology including the presence of specialized tissue types and distinct anatomical features, gene repertoires and networks, as well as the habitat differ significantly from those of vascular plants. To evaluate the outcomes of these differences, we explore the phenotypic responses of mosses to environmental signals such as light, temperature, CO2, water, nutrients, and gravity, and compare those with what is known in vascular plants. We also outline knowledge gaps and formulate testable hypotheses based on the contribution of anatomical and molecular factors to specific phenotypic responses.Cellular proliferation depends on the accurate and timely replication of the genome. Several genetic diseases are caused by mutations in key DNA replication genes; however, it remains unclear whether these genes influence the normal program of DNA replication timing. Similarly, the factors that regulate DNA replication dynamics are poorly understood. To systematically identify trans-acting modulators of replication timing, we profiled replication in 184 cell lines from three cell types, encompassing 60 different gene knockouts or genetic diseases. Through a rigorous approach that considers the background variability of replication timing, we concluded that most samples displayed normal replication timing. However, mutations in two genes showed consistently abnormal replication timing. The first gene was RIF1, a known modulator of replication timing. The second was MCM10, a highly conserved member of the pre-replication complex. Cells from a single patient carrying MCM10 mutations demonstrated replication timing variability comprising 46% of the genome and at different locations than RIF1 knockouts.