Intricate environment-modulated genetic networks control isoflavone accumulation in soybean seeds

<p>Abstract</p> <p>Background</p> <p>Soybean (<it>Glycine max </it>[L] Merr.) seed isoflavones have long been considered a desirable trait to target in selection programs for their contribution to human health and plant defense systems. However, attempts to modify seed isoflavone contents have not always produced the expected results because their genetic basis is polygenic and complex. Undoubtedly, the extreme variability that seed isoflavones display over environments has obscured our understanding of the genetics involved.</p> <p>Results</p> <p>In this study, a mapping population of RILs with three replicates was analyzed in four different environments (two locations over two years). We found a total of thirty-five main-effect genomic regions and many epistatic interactions controlling genistein, daidzein, glycitein and total isoflavone accumulation in seeds. The use of distinct environments permitted detection of a great number of environment-modulated and minor-effect QTL. Our findings suggest that isoflavone seed concentration is controlled by a complex network of multiple minor-effect loci interconnected by a dense epistatic map of interactions. The magnitude and significance of the effects of many of the nodes and connections in the network varied depending on the environmental conditions. In an attempt to unravel the genetic architecture underlying the traits studied, we searched on a genome-wide scale for genomic regions homologous to the most important identified isoflavone biosynthetic genes. We identified putative candidate genes for several of the main-effect and epistatic QTL and for QTL reported by other groups.</p> <p>Conclusions</p> <p>To better understand the underlying genetics of isoflavone accumulation, we performed a large scale analysis to identify genomic regions associated with isoflavone concentrations. We not only identified a number of such regions, but also found that they can interact with one another and with the environment to form a complex adaptable network controlling seed isoflavone levels. We also found putative candidate genes in several regions and overall we advanced the knowledge of the genetics underlying isoflavone synthesis.</p

Linkage analysis and residual heterozygotes derived near isogenic lines reveals a novel protein quantitative trait loci from a Glycine soja accession

Modern soybean [Glycine max (L.) Merr] cultivars have low overall genetic variation due to repeated bottleneck events that arose during domestication and from selection strategies typical of many soybean breeding programs. In both public and private soybean breeding programs, the introgression of wild soybean (Glycine soja Siebold and Zucc.) alleles is a viable option to increase genetic diversity and identify new sources for traits of value. The objectives of our study were to examine the genetic architecture responsible for seed protein and oil using a recombinant inbred line (RIL) population derived from hybridizing a G. max line (‘Osage’) with a G. soja accession (PI 593983). Linkage mapping identified a total of seven significant quantitative trait loci on chromosomes 14 and 20 for seed protein and on chromosome 8 for seed oil with LOD scores ranging from 5.3 to 31.7 for seed protein content and from 9.8 to 25.9 for seed oil content. We analyzed 3,015 single F4:9 soybean plants to develop two residual heterozygotes derived near isogenic lines (RHD-NIL) populations by targeting nine SNP markers from genotype-by-sequencing, which corresponded to two novel quantitative trait loci (QTL) derived from G. soja: one for a novel seed oil QTL on chromosome 8 and another for a novel protein QTL on chromosome 14. Single marker analysis and linkage analysis using 50 RHD-NILs validated the chromosome 14 protein QTL, and whole genome sequencing of RHD-NILs allowed us to reduce the QTL interval from ∼16.5 to ∼4.6 Mbp. We identified two genomic regions based on recombination events which had significant increases of 0.65 and 0.72% in seed protein content without a significant decrease in seed oil content. A new Kompetitive allele-specific polymerase chain reaction (KASP) assay, which will be useful for introgression of this trait into modern elite G. max cultivars, was developed in one region. Within the significantly associated genomic regions, a total of eight genes are considered as candidate genes, based on the presence of gene annotations associated with the protein or amino acid metabolism/movement. Our results provide better insights into utilizing wild soybean as a source of genetic diversity for soybean cultivar improvement utilizing native traits

JWST and ALMA discern the assembly of structural and obscured components in a high-redshift starburst galaxy

We present observations and analysis of the starburst, PACS-819, at z=1.45 ($M_*=10^{10.7}$ M$_{ \odot}$), using high-resolution ($0^{\prime \prime}.1$; 0.8 kpc) ALMA and multi-wavelength JWST images from the COSMOS-Web program. Dissimilar to HST/ACS images in the rest-frame UV, the redder NIRCam and MIRI images reveal a smooth central mass concentration and spiral-like features, atypical for such an intense starburst. Through dynamical modeling of the CO J=5--4 emission with ALMA, PACS-819 is rotation-dominated thus has a disk-like nature. However, kinematic anomalies in CO and asymmetric features in the bluer JWST bands (e.g., F150W) support a more disturbed nature likely due to interactions. The JWST imaging further enables us to map the distribution of stellar mass and dust attenuation, thus clarifying the relationships between different structural components, not discernable in the previous HST images. The CO J = 5 -- 4 and FIR dust continuum emission are co-spatial with a heavily-obscured starbursting core (<1 kpc) which is partially surrounded by much less obscured star-forming structures including a prominent arc, possibly a tidally-distorted dwarf galaxy, and a clump, either a sign of an ongoing violent disk instability or a recently accreted low-mass satellite. With spatially-resolved maps, we find a high molecular gas fraction in the central area reaching $\sim3$ ($M_{\text{gas}}$/$M_*$) and short depletion times ($M_{\text{gas}}/SFR\sim$ 120 Myrs) across the entire system. These observations provide insights into the complex nature of starbursts in the distant universe and underscore the wealth of complementary information from high-resolution observations with both ALMA and JWST.Comment: 18 pages, 12 figures, Submitted to Ap

Signal transducer and activator of transcription 1 (STAT1) gain-of-function mutations and disseminated coccidioidomycosis and histoplasmosis

Background: Impaired signaling in the IFN-g/IL-12 pathway causes susceptibility to severe disseminated infections with mycobacteria and dimorphic yeasts. Dominant gain-of-function mutations in signal transducer and activator of transcription 1 (STAT1) have been associated with chronic mucocutaneous candidiasis. Objective: We sought to identify the molecular defect in patients with disseminated dimorphic yeast infections. Methods: PBMCs, EBV-transformed B cells, and transfected U3A cell lines were studied for IFN-g/IL-12 pathway function. STAT1 was sequenced in probands and available relatives. Interferon-induced STAT1 phosphorylation, transcriptional responses, protein-protein interactions, target gene activation, and function were investigated. Results: We identified 5 patients with disseminated Coccidioides immitis or Histoplasma capsulatum with heterozygous missense mutations in the STAT1 coiled-coil or DNA-binding domains. These are dominant gain-of-function mutations causing enhanced STAT1 phosphorylation, delayed dephosphorylation, enhanced DNA binding and transactivation, and enhanced interaction with protein inhibitor of activated STAT1. The mutations caused enhanced IFN-g–induced gene expression, but we found impaired responses to IFN-g restimulation. Conclusion: Gain-of-function mutations in STAT1 predispose to invasive, severe, disseminated dimorphic yeast infections, likely through aberrant regulation of IFN-g–mediated inflammationFil: Sampaio, Elizabeth P.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados Unidos. Instituto Oswaldo Cruz. Laboratorio de Leprologia; BrasilFil: Hsu, Amy P.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Pechacek, Joseph. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Hannelore I.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados Unidos. Erasmus Medical Center. Department of Medical Microbiology and Infectious Disease; Países BajosFil: Dias, Dalton L.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Paulson, Michelle L.. Clinical Research Directorate/CMRP; Estados UnidosFil: Chandrasekaran, Prabha. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Rosen, Lindsey B.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Carvalho, Daniel S.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados Unidos. Instituto Oswaldo Cruz, Laboratorio de Leprologia; BrasilFil: Ding, Li. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Vinh, Donald C.. McGill University Health Centre. Division of Infectious Diseases; CanadáFil: Browne, Sarah K.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Datta, Shrimati. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Allergic Diseases. Allergic Inflammation Unit; Estados UnidosFil: Milner, Joshua D.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Allergic Diseases. Allergic Inflammation Unit; Estados UnidosFil: Kuhns, Douglas B.. Clinical Services Program; Estados UnidosFil: Long Priel, Debra A.. Clinical Services Program; Estados UnidosFil: Sadat, Mohammed A.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Host Defenses. Infectious Diseases Susceptibility Unit; Estados UnidosFil: Shiloh, Michael. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: De Marco, Brendan. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: Alvares, Michael. University of Texas. Southwestern Medical Center. Division of Allergy and Immunology; Estados UnidosFil: Gillman, Jason W.. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: Ramarathnam, Vivek. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: de la Morena, Maite. University of Texas. Southwestern Medical Center. Division of Allergy and Immunology; Estados UnidosFil: Bezrodnik, Liliana. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Ricardo Gutierrez"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Moreira, Ileana. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Ricardo Gutierrez"; ArgentinaFil: Uzel, Gulbu. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Johnson, Daniel. University of Chicago. Comer Children; Estados UnidosFil: Spalding, Christine. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Zerbe, Christa S.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Wiley, Henry. National Eye Institute. Clinical Trials Branch; Estados UnidosFil: Greenberg, David E.. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: Hoover, Susan E.. University of Arizona. College of Medicine. Valley Fever Center for Excellence; Estados UnidosFil: Rosenzweig, Sergio D.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Host Defenses Infectious Diseases Susceptibility Unit; Estados Unidos. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Primary Immunodeficiency Clinic; Estados UnidosFil: Galgiani, John N.. University of Arizona. College of Medicine. Valley Fever Center for Excellence; Estados UnidosFil: Holland, Steven M.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados Unido

COSMOS-Web: Intrinsically Luminous z≳\gtrsim10 Galaxy Candidates Test Early Stellar Mass Assembly

We report the discovery of 15 exceptionally luminous $10\lesssim z\lesssim14$ candidate galaxies discovered in the first 0.28 deg$^2$ of JWST/NIRCam imaging from the COSMOS-Web Survey. These sources span rest-frame UV magnitudes of $-20.5>M_{\rm UV}>-22$, and thus constitute the most intrinsically luminous $z\gtrsim10$ candidates identified by JWST to-date. Selected via NIRCam imaging with Hubble ACS/F814W, deep ground-based observations corroborate their detection and help significantly constrain their photometric redshifts. We analyze their spectral energy distributions using multiple open-source codes and evaluate the probability of low-redshift solutions; we conclude that 12/15 (80%) are likely genuine $z\gtrsim10$ sources and 3/15 (20%) likely low-redshift contaminants. Three of our $z\sim12$ candidates push the limits of early stellar mass assembly: they have estimated stellar masses $\sim5\times10^{9}\,M_\odot$, implying an effective stellar baryon fraction of $\epsilon_{\star}\sim0.2-0.5$, where $\epsilon_{\star}\equiv M_{\star}/(f_{b}M_{halo})$. The assembly of such stellar reservoirs is made possible due to rapid, burst-driven star formation on timescales $<$100\,Myr where the star-formation rate may far outpace the growth of the underlying dark matter halos. This is supported by the similar volume densities inferred for $M_\star\sim10^{10}\,M_\odot$ galaxies relative to $M_\star\sim10^{9}\,M_\odot$ -- both about $10^{-6}$ Mpc$^{-3}$ -- implying they live in halos of comparable mass. At such high redshifts, the duty cycle for starbursts would be of order unity, which could cause the observed change in the shape of the UVLF from a double powerlaw to Schechter at $z\approx8$. Spectroscopic redshift confirmation and ensuing constraints of their masses will be critical to understanding how, and if, such early massive galaxies push the limits of galaxy formation in $\Lambda$CDM.Comment: 30 pages, 9 figures; ApJ submitte

Uncovering a Massive z~7.65 Galaxy Hosting a Heavily Obscured Radio-Loud QSO Candidate in COSMOS-Web

In this letter, we report the discovery of the highest redshift, heavily obscured, radio-loud QSO candidate selected using JWST NIRCam/MIRI, mid-IR, sub-mm, and radio imaging in the COSMOS-Web field. Using multi-frequency radio observations and mid-IR photometry, we identify a powerful, radio-loud (RL), growing supermassive black hole (SMBH) with significant spectral steepening of the radio SED ($f_{1.32 \mathrm{GHz}} \sim 2$ mJy, $q_{24\mu m} = -1.1$, $\alpha_{1.32-3\mathrm{GHz}}=-1.2$, $\Delta \alpha = -0.4$). In conjunction with ALMA, deep ground-based observations, ancillary space-based data, and the unprecedented resolution and sensitivity of JWST, we find no evidence of QSO contribution to the UV/optical/NIR data and thus infer heavy amounts of obscuration (N$_{\mathrm{H}} > 10^{23}$ cm$^{-2}$). Using the wealth of deep UV to sub-mm photometric data, we report a singular solution photo-z of $z_\mathrm{phot}$ = 7.65$^{+0.4}_{-0.3}$ and estimate an extremely massive host-galaxy ($\log M_{\star} = 11.92 \pm 0.06\,\mathrm{M}_{\odot}$). This source represents the furthest known obscured RL QSO candidate, and its level of obscuration aligns with the most representative but observationally scarce population of QSOs at these epochs.Comment: Submitted to ApJL, Comments welcom

Unveiling the distant Universe: Characterizing z≥9z\ge9 Galaxies in the first epoch of COSMOS-Web

We report the identification of 15 galaxy candidates at $z\ge9$ using the initial COSMOS-Web JWST observations over 77 arcmin$^2$ through four NIRCam filters (F115W, F150W, F277W, F444W) with an overlap with MIRI (F770W) of 8.7 arcmin$^2$. We fit the sample using several publicly-available SED fitting and photometric redshift codes and determine their redshifts between $z=9.3$ and $z=10.9$ ($\langle z\rangle=10.0$), UV-magnitudes between M$_{\rm UV}$ = $-$21.2 and $-$19.5 (with $\langle$M$_{\rm UV}\rangle=-20.2$) and rest-frame UV slopes ($\langle \beta\rangle=-2.4$). These galaxies are, on average, more luminous than most $z\ge9$ candidates discovered by JWST so far in the literature, while exhibiting similar blue colors in their rest-frame UV. The rest-frame UV slopes derived from SED-fitting are blue ($\beta\sim$[$-$2.0, $-$2.7]) without reaching extremely blue values as reported in other recent studies at these redshifts. The blue color is consistent with models that suggest the underlying stellar population is not yet fully enriched in metals like similarly luminous galaxies in the lower redshift Universe. The derived stellar masses with $\langle \log_{\rm 10} ($M$_\star/$M$_\odot)\rangle\approx8-9$ are not in tension with the standard $\Lambda$CDM model and our measurement of the volume density of such UV luminous galaxies aligns well with previously measured values presented in the literature at $z\sim9-10$. Our sample of galaxies, although compact, are significantly resolved.Comment: Submitted to Ap