Gene expression data from isolated stele cells after roots were treated with 140 mM NaCl for 20 hour Data quality was examined using the signal distribution of Affymetrix built-in controls (Spike-in and hybridization controls) using Expression Console software (Affymetrix) and AffyQCReport. GCRMA in R/Bioconductor was used for data normalization.

Gene expression data from isolated stele cells after roots were treated with 140 mM NaCl for 32 hour Data quality was examined using the signal distribution of Affymetrix built-in controls (Spike-in and hybridization controls) using Expression Console software (Affymetrix) and AffyQCReport. GCRMA in R/Bioconductor was used for data normalization.

Spatially resolved images of debris discs are necessary to determine disc morphological properties and the scattering phase function (SPF) thatantifies the brightness of scattered light as a function of phase angle. Current high-contrast imaging instruments have successfully resolved several dozens of debris discs around other stars, but few studies have investigated trends in the scattered-light, resolved population of debris discs in a uniform and consistent manner. We have combined Karhunen-Loeve Image Projection (KLIP) with radiative-transfer disc forward modelling in order to obtain the highest-quality image reductions and constrain disc morphological properties of eight debris discs imaged by the Gemini Planet Imager at H-band with a consistent and uniformly applied approach. In describing the scattering properties of our models, we assume a common SPF informed from solar system dust scattering measurements and apply it to all systems. We identify a diverse range of dust density properties among the sample, including critical radius, radial width, and vertical width. We also identify radially narrow and vertically extended discs that may have resulted from substellar companion perturbations, along with a tentative positive trend in disc eccentricity with relative disc width. We also find that using a common SPF can achieve reasonable model fits for discs that are axisymmetric and asymmetric when fitting models to each side of the disc independently, suggesting that scattering behaviour from debris discs may be similar to Solar system dust.

Introduction Sida fallax (Malvaceae) is the most widespread and variable taxon of Malvaceae in the Hawaiian Islands, growing with a diversity of morphological forms in different habitats including Midway Atoll, Nihoa, and all the main islands. Morphological variation exists within and among populations. The study aimed to investigate the genetic variation within and among populations from various habitats and geographic locations throughout the Hawaiian range of S. fallax. Methods A total of 124 samples, with up to five samples per population where possible, were collected from 26 populations across six of the main Hawaiian Islands (KauaModified Letter Turned Commai, OModified Letter Turned Commaahu, Maui, MolokaModified Letter Turned Commai, LanaModified Letter Turned Commai, and HawaiModified Letter Turned Commai) and Nihoa in the Northwestern Hawaiian Islands. The sampling strategy encompassed collecting populations from different habitats and geographic locations, including coastal and mountain ecotypes, with many intermediate morphological forms. Multiplexed ISSR genotyping by sequencing (MIG-seq) was used to detect single nucleotide polymorphisms (SNP) and genetic differences among individuals and populations were evaluated using PCO analyses. Results The relationship of FST with the geographical distance between the populations was assessed using the Mantel test. The results showed that populations on a single island were more closely related to each other and to populations on islands within their respective groups than they were to populations on other islands. Discussion The overall genetic relationships among islands were, to a large extent, predictive based on island position within the chain and, to a lesser extent, within island topography.

Light-harvesting complex stress-related protein 3 (LHCSR3) expression is observed in various protoxidizing conditions like high light and nutrient starvation. LHCSR3 expression is essential for energy-dependent quenching (qE), whereas its role under nutrient starvation is elusive. It is also unclear how nutrient starvation can induce LHCSR3 expression under subsaturating light intensities. To study the role of LHCSR3 under nutrient starvation, the C. reinhardtii cells are grown under osmotic stress that would prevent water uptake; therefore same holds true for soluble nutrients in the medium. In this work, we have shown that LHCSR3 expression can occur under osmotic stress and subsaturating light intensities, whereas it does not elicit qE. Further examination of thylakoid membrane architecture from wild-type and npq4 mutant grown under nutrient starvation revealed that LHCSR3 expression affects the interaction between the PSII core with its peripheral LHCII antenna and possibly can prevent excitation energy transfer. Thylakoid lumen acidification is essential for the expression and function of LHCSR3. Under saturating light intensities, this is achieved by the increased rate of photosynthetic electron flow coupled with proton translocation into the thylakoid lumen. Whereas, under nutrient starvation, the reports of LHCSR3 expression also showed reduced photosynthetic electron flow. Therefore, an alternative mechanism should exist for developing the proton gradient. We observed the downregulation of chloroplast (cp) ATP synthase activity and its abundance under osmotic stress, suggesting the role of (cp) ATP synthase in thylakoid lumen acidification under reduced photosynthetic electron flow. This observation is supported by the expression of LHCSR3 in (cp) ATP-synthase mutant atpF upon exposure to moderate light intensity. This study proposes that the mechanism of LHCSR3 expression and its functionality can vary with the type of photooxidizing stress.

Little is known about how the spectrum and etiology of germline mutagenesis might vary among mammalian species. To shed light on this mystery, we quantify variation in mutational sequence context biases using polymorphism data from thirteen species of mice, apes, bears, wolves, and cetaceans. After normalizing the mutation spectrum for reference genome accessibility and k -mer content, we use the Mantel test to deduce that mutation spectrum divergence is highly correlated with genetic divergence between species, whereas life history traits like reproductive age are weaker predictors of mutation spectrum divergence. Potential bioinformatic confounders are only weakly related to a small set of mutation spectrum features. We find that clocklike mutational signatures previously inferred from human cancers cannot explain the phylogenetic signal exhibited by the mammalian mutation spectrum, despite the ability of these clocklike signatures to fit each species' 3-mer spectrum with high cosine similarity. In contrast, parental aging signatures inferred from human de novo mutation data appear to explain much of the mutation spectrum's phylogenetic signal when fit to non-context-dependent mutation spectrum data in combination with a novel mutational signature. We posit that future models purporting to explain the etiology of mammalian mutagenesis need to capture the fact that more closely related species have more similar mutation spectra; a model that fits each marginal spectrum with high cosine similarity is not guaranteed to capture this hierarchy of mutation spectrum variation among species.

Although evolutionary biologists have long theorized that variation in DNA repair efficacy might explain some of the diversity of lifespan and cancer incidence across species, we have little data on the variability of normal germline mutagenesis outside of humans. Here, we shed light on the spectrum and etiology of mutagenesis across mammals by quantifying mutational sequence context biases using polymorphism data from thirteen species of mice, apes, bears, wolves, and cetaceans. After normalizing the mutation spectrum for reference genome accessibility and k-mer content, we use the Mantel test to deduce that mutation spectrum divergence is highly correlated with genetic divergence between species, whereas life history traits like reproductive age are weaker predictors of mutation spectrum divergence. Potential bioinformatic confounders are only weakly related to a small set of mutation spectrum features. We find that clock-like mutational signatures previously inferred from human cancers cannot explain the phylogenetic signal exhibited by the mammalian mutation spectrum, despite the ability of these signatures to fit each species' 3-mer spectrum with high cosine similarity. In contrast, parental aging signatures inferred from human de novo mutation data appear to explain much of the 1-mer spectrum's phylogenetic signal in combination with a novel mutational signature. We posit that future models purporting to explain the etiology of mammalian mutagenesis need to capture the fact that more closely related species have more similar mutation spectra; a model that fits each marginal spectrum with high cosine similarity is not guaranteed to capture this hierarchy of mutation spectrum variation among species.