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Purpose: The response of rice (Oryza sativa L.) plants to phosphorus (P) deficiency and to alterations in the rhizosphere microbiome in flooded soils remains unexplored. We aimed to identify the association between alterations in bacterial diversity and underground metabolic and chemical reactions in the rhizosphere in P-deficient and γ-irradiated conditions. Methods: Two rice varieties were grown in a split-root box under flooded conditions and filled with either P-applied or non-P-applied soils with or without γ-irradiation. At 41–42 days after transplanting, we determined plant biomass, P uptake, exudation rates of total carbon and low-molecular-weight organic acids (LMWOAs) from the roots, and bacterial diversity, P fractions, and phosphatase activity in the rhizosphere. Results: γ-irradiation significantly decreased the P uptake and biomass of both rice varieties and reduced the relative abundance of Alphaproteobacteria and microbiome beta diversity in the rhizosphere. Concurrently, γ-irradiation reduced the uptake of insoluble P from soils. These microbiological and chemical changes in the γ-irradiated rhizosphere occurred irrespective of the P treatments of soils. On the contrary, the proportion of LMWOAs and citric acid exudation, which have a high P-solubilization capacity, increased in the γ-irradiated and P-applied rhizosphere soils at the expense of other carbons. No differences were detected in phosphatase activity in any treatments. Conclusion: Dysbiosis of the rhizosphere microbiome negatively affected rice growth and the uptake of insoluble P in flooded soils. With a reduction in microbiome diversity, rice plants may have a complementary strategy to increase the proportion of citric acid exudation toward the P-rich soil area. [ABSTRACT FROM AUTHOR]

Improved phosphorus (P) use efficiency for crop production is needed, given the depletion of phosphorus ore deposits, and increasing ecological concerns about its excessive use. Root system architecture (RSA) is important in efficiently capturing immobile P in soils, while agronomically, localized P application near the roots is a potential approach to address this issue. However, the interaction between genetic traits of RSA and localized P application has been little understood. Near-isogenic lines (NILs) and their parent of rice (qsor1-NIL, Dro1-NIL, and IR64, with shallow, deep, and intermediate root growth angles (RGA), respectively) were grown in flooded pots after placing P near the roots at transplanting (P-dipping). The experiment identified that the P-dipping created an available P hotspot at the plant base of the soil surface layer where the qsor1-NIL had the greatest root biomass and root surface area despite no genotyipic differences in total values, whereby the qsor1-NIL had significantly greater biomass and P uptake than the other genotypes in the P-dipping. The superior surface root development of qsor1-NIL could have facilitated P uptakes from the P hotspot, implying that P-use efficiency in crop production can be further increased by combining genetic traits of RSA and localized P application. [ABSTRACT FROM AUTHOR]

The genetic improvement of drought resistance is essential for stable and adequate crop production in drought-prone areas. Here we demonstrate that alteration of root system architecture improves drought avoidance through the cloning and characterization of DEEPER ROOTING 1 (DRO1), a rice quantitative trait locus controlling root growth angle. DRO1 is negatively regulated by auxin and is involved in cell elongation in the root tip that causes asymmetric root growth and downward bending of the root in response to gravity. Higher expression of DRO1 increases the root growth angle, whereby roots grow in a more downward direction. Introducing DRO1 into a shallow-rooting rice cultivar by backcrossing enabled the resulting line to avoid drought by increasing deep rooting, which maintained high yield performance under drought conditions relative to the recipient cultivar. Our experiments suggest that control of root system architecture will contribute to drought avoidance in crops. [ABSTRACT FROM AUTHOR]

Leaf photosynthesis, an important determinant of yield potential in rice, can be estimated from measurements of chlorophyll content. We searched for quantitative trait loci (QTLs) for Soil and Plant Analyzer Development (SPAD) value, an index of leaf chlorophyll content, and assessed their association with leaf photosynthesis. QTL analysis derived from a cross between japonica cultivar Sasanishiki and high-yielding indica cultivar Habataki detected a QTL for SPAD value on chromosome 4. This QTL explained 31% of the total phenotypic variance, and the Habataki allele increased the SPAD value. Chromosomal segment substitution line (CSSL) with the corresponding segment from Habataki had a higher leaf photosynthetic rate and SPAD value than Sasanishiki, suggesting an association between SPAD value and leaf photosynthesis. The CSSL also had a lower specific leaf area (SLA) than Sasanishiki, reflecting its thicker leaves. Substitution mapping under Sasanishiki genetic background demonstrated that QTLs for SPAD value and SLA were co-localized in the 1,798-kb interval. The results suggest that the phenotypes for SPAD value and SLA are controlled by a single locus or two tightly linked loci, and may play an important role in increasing leaf photosynthesis by increasing chlorophyll content or leaf thickness, or both. [ABSTRACT FROM AUTHOR]

Macrophage colony-stimulating factor (M-CSF) influences the proliferation and survival of mononuclear phagocytes through the receptor CSF-1R. The adaptor protein DAP12 is critical for the function of mononuclear phagocytes. DAP12-mutant mice and humans have defects in osteoclasts and microglia, as well as brain and bone abnormalities. Here we show DAP12 deficiency impaired the M-CSF-induced proliferation and survival of macrophages in vitro. DAP12-deficient mice had fewer microglia in defined central nervous system areas, and DAP12-deficient progenitors regenerated myeloid cells inefficiently after bone marrow transplantation. Signaling by M-CSF through CSF-1R induced the stabilization and nuclear translocation of β-catenin, which activated genes involved in the cell cycle. DAP12 was essential for phosphorylation and nuclear accumulation of β-catenin. Our results provide a mechanistic explanation for the many defects of DAP12-deficient mononuclear phagocytes. [ABSTRACT FROM AUTHOR]

Increasing leaf photosynthesis offers a possible way to improve yield potential in rice ( Oryza sativa L.). Carbon isotope discrimination (Δ13C) has potential as an indirect selection criterion. In this study, we searched for quantitative trait loci (QTLs) controlling Δ13C, and assessed their association with leaf photosynthesis. Substitution mapping by using chromosome segment substitution lines (CSSLs), that carry segments from the indica cultivar Kasalath in the genetic background of the japonica cultivar Koshihikari, identified genomic regions affecting Δ13C on chromosomes (Chr.) 2, 3, 6, 7, and 12. One of the CSSLs, SL208, in which most regions on Chr. 3 were substituted with Kasalath segments, showed higher leaf stomatal conductance for CO2 ( gs) and Δ13C than Koshihikari during the vegetative stage although leaf photosynthetic rate did not differ between them. These results suggest an association between Δ13C and gs. To test this association, we performed a QTL analysis for Δ13C at vegetative and heading stages in an F2 population derived from a cross between SL208 and Koshihikari. The results confirmed a QTL controlling Δ13C on the long arm of Chr. 3. By using a near-isogenic line specific to Hd6, we ruled out the possibility that variation in Δ13C was generated through the pleiotropic effect of heading date. [ABSTRACT FROM AUTHOR]

The Fc receptor common γ-chain (FcRγ) is a widely expressed adaptor bearing an immunoreceptor tyrosine-based activation motif (ITAM) that transduces activation signals from various immunoreceptors. We show here that basophils lacking FcRγ developed normally and proliferated efficiently in response to interleukin 3 (IL-3) but were very impaired in IL-3-induced production of IL-4 and in supporting T helper type 2 differentiation. Through its transmembrane portion, FcRγ associated constitutively with the common β-chain of the IL-3 receptor and signaled by recruiting the kinase Syk. Retrovirus-mediated complementation demonstrated the essential function of the ITAM of FcRγ in IL-3 signal transduction. Our results identify a previously unknown mechanism whereby FcRγ functions to 'route' selective cytokine-triggered signals into the ITAM-mediated IL-4 production pathway. [ABSTRACT FROM AUTHOR]

Immunoreceptor tyrosine-based activation motifs (ITAMs) are crucial in antigen receptor signaling in acquired immunity. Although receptors associated with the ITAM-bearing adaptors FcRγ and DAP12 on myeloid cells have been suggested to activate innate immune responses, the mechanism coupling those receptors to 'downstream' signaling events is unclear. The CARMA1–Bcl-10–MALT1 complex is critical for the activation of transcription factor NF-κB in lymphocytes but has an unclear function in myeloid cells. Here we report that deletion of the gene encoding the Bcl-10 adaptor–binding partner CARD9 resulted in impaired myeloid cell activation of NF-κB signaling by several ITAM-associated receptors. Moreover, CARD9 was required for Toll-like receptor–induced activation of dendritic cells through the activation of mitogen-activated protein kinases. Although Bcl10−/− and Card9−/− mice had similar signaling impairment in myeloid cells, Card11−/− (CARMA1-deficient) myeloid cell responses were normal, and although Card11−/− lymphocytes were defective in antigen receptor–mediated activation, Card9−/− lymphocytes were not. Thus, the activation of lymphoid and myeloid cells through ITAM-associated receptors or Toll-like receptors is regulated by CARMA1–Bcl-10 and CARD9–Bcl-10, respectively. [ABSTRACT FROM AUTHOR]

Calcium (Ca2+) signaling is essential for a variety of cellular responses and higher biological functions. Ca2+/calmodulin-dependent kinases (CaMKs) and the phosphatase calcineurin activate distinct downstream pathways that are mediated by the transcription factors cAMP response element (CRE)-binding protein (CREB) and nuclear factor of activated T cells (NFAT), respectively. The importance of the calcineurin-NFAT pathway in bone metabolism has been demonstrated in osteoclasts, osteoblasts and chondrocytes. However, the contribution of the CaMK-CREB pathway is poorly understood, partly because of the difficulty of dissecting the functions of homologous family members. Here we show that the CaMKIV-CREB pathway is crucial for osteoclast differentiation and function. Pharmacological inhibition of CaMKs as well as the genetic ablation of Camk4 reduced CREB phosphorylation and downregulated the expression of c-Fos, which is required for the induction of NFATc1 (the master transcription factor for osteoclastogenesis) that is activated by receptor activator of NF-κB ligand (RANKL). Furthermore, CREB together with NFATc1 induced the expression of specific genes expressed by differentiated osteoclasts. Thus, the CaMK-CREB pathway biphasically functions to regulate the transcriptional program of osteoclastic bone resorption, by not only enhancing induction of NFATc1 but also facilitating NFATc1-dependent gene regulation once its expression is induced. This provides a molecular basis for a new therapeutic strategy for bone diseases. [ABSTRACT FROM AUTHOR]

Semaphorins and their receptors have diverse functions in axon guidance, organogenesis, vascularization and/or angiogenesis, oncogenesis and regulation of immune responses. The primary receptors for semaphorins are members of the plexin family. In particular, plexin-A1, together with ligand-binding neuropilins, transduces repulsive axon guidance signals for soluble class III semaphorins, whereas plexin-A1 has multiple functions in chick cardiogenesis as a receptor for the transmembrane semaphorin, Sema6D, independent of neuropilins. Additionally, plexin-A1 has been implicated in dendritic cell function in the immune system. However, the role of plexin-A1 in vivo, and the mechanisms underlying its pleiotropic functions, remain unclear. Here, we generated plexin-A1-deficient (plexin-A1−/−) mice and identified its important roles, not only in immune responses, but also in bone homeostasis. Furthermore, we show that plexin-A1 associates with the triggering receptor expressed on myeloid cells-2 (Trem-2), linking semaphorin-signalling to the immuno-receptor tyrosine-based activation motif (ITAM)-bearing adaptor protein, DAP12. These findings reveal an unexpected role for plexin-A1 and present a novel signalling mechanism for exerting the pleiotropic functions of semaphorins. [ABSTRACT FROM AUTHOR]

Immune responses are often regulated by opposing receptor pairs that recognize the same ligand but deliver either activating or inhibitory signals. Paired immunoglobulin-like receptors (PIRs) expressed on B cells and myeloid cells comprise a major histocompatibility complex class I recognition system that regulates the responsiveness of these cells. Here, activating PIR-A and inhibitory PIR-B bound various mouse major histocompatibility complex class I (H-2) molecules, and in vitro H-2 tetramer stimulation of PIR-B on B cells or PIR-A on macrophages induced intracellular phosphotyrosine signaling. After transfer of allogeneic splenocytes into PIR-B-deficient mice, the mice showed exacerbated graft-versus-host disease, which was due to augmented activation of recipient dendritic cells with concomitant upregulation of PIR-A and increased interferon-? production. PIR-A-induced dendritic cell activation also led to increased proliferation of donor cytotoxic T cells. Thus, PIR-A and PIR-B are counteracting receptors that are essential for successful tissue transplantation and may regulate irrelevant reaction to autologous tissues in a constitutive way in physiological conditions. [ABSTRACT FROM AUTHOR]

Costimulatory signals are required for activation of immune cells, but it is not known whether they contribute to other biological systems. The development and homeostasis of the skeletal system depend on the balance between bone formation and resorption. Receptor activator of NF-?B ligand (RANKL) regulates the differentiation of bone-resorbing cells, osteoclasts, in the presence of macrophage-colony stimulating factor (M-CSF). But it remains unclear how RANKL activates the calcium signals that lead to induction of nuclear factor of activated T cells c1, a key transcription factor for osteoclastogenesis. Here we show that mice lacking immunoreceptor tyrosine-based activation motif (ITAM)-harbouring adaptors, Fc receptor common ? subunit (FcR?) and DNAX-activating protein (DAP)12, exhibit severe osteopetrosis owing to impaired osteoclast differentiation. In osteoclast precursor cells, FcR? and DAP12 associate with multiple immunoreceptors and activate calcium signalling through phospholipase C?. Thus, ITAM-dependent costimulatory signals activated by multiple immunoreceptors are essential for the maintenance of bone homeostasis. These results reveal that RANKL and M-CSF are not sufficient to activate the signals required for osteoclastogenesis. [ABSTRACT FROM AUTHOR]

The receptors for the Fc of immunoglobulins, Fc receptors (FcRs), link the humoral and cellular branches of the immune system, and they have important functions in the activation and down-modulation of immune responses. Balanced signalling through activating and inhibitory FcRs regulates the activity of various cells in the immune system. Recent work in animal models indicates that the development of many human autoimmune diseases might be caused by impairment of the FcR regulatory system. This review provides an overview of the mechanisms of FcR-based immune regulation and describes how autoimmune disease might result from its dysfunction. [ABSTRACT FROM AUTHOR]

Mice deficient for paired immunoglobulin (Ig)-like receptor B (PIR-B) show defective regulation of receptor-mediated activation in antigen-presenting cells. Older PIR-B-/- mice had an increased number of peritoneal B1 cells. Splenic PIR-B-/- B2 cells were constitutively activated and proliferated much more than those from wild-type mice upon B cell receptor ligation. T helper type 2 (TH2)-prone humoral responses were augmented in PIR-B-/- mice upon immunization with T-dependent antigens, including increased interleukin 4 and decreased interferon-? responses, as well as enhanced IgG1 and IgE production. Impaired maturation of dendritic cells (DCs), possibly due to perturbed intracellular signaling, was responsible for the skewed responses. Thus, PIR-B is critical for B cell suppression, DC maturation and for balancing TH1 and TH2 immune responses. [ABSTRACT FROM AUTHOR]

Examines the augmented humoral and anaphylactic responses in FcgammaRII-deficient mice. Display of elevated immunoglobin levels of FcgammaRII-deficient animals; Sensitivity of mast cells from FcgammaRII -/- to IgG-triggered degranulation; FcgammaRII as a negative regulator of immune-complex-triggered activation in vivo for both the afferent and efferent limbs of the immune response.

The pathway of homeostatic IgG extravasation is not fully understood, in spite of its importance for the maintenance of host immunity, the management of autoantibody-mediated disorders, and the use of antibody-based biologics. Here we show in a murine model of pemphigus, a prototypic cutaneous autoantibody-mediated disorder, that blood-circulating IgG extravasates into the skin in a time- and dose-dependent manner under homeostatic conditions. This IgG extravasation is unaffected by depletion of Fcγ receptors, but is largely attenuated by specific ablation of dynamin-dependent endocytic vesicle formation in blood endothelial cells (BECs). Among dynamin-dependent endocytic vesicles, IgG co-localizes well with caveolae in cultured BECs. An Abl family tyrosine kinase inhibitor imatinib, which reduces caveolae-mediated endocytosis, impairs IgG extravasation in the skin and attenuates the murine pemphigus manifestations. Our study highlights the kinetics of IgG extravasation in vivo, which might be a clue to understand the pathological mechanism of autoantibody-mediated autoimmune disorders. How antibody reaches tissues from circulation is critical for understanding antibody-mediated immunity. Here the authors show that IgG extravasation in the skin is mediated by endothelial caveolin transport independently of FcR, and is targetable by imatinib, which reduces IgG-dependent pathology in a mouse model of pemphigus. [ABSTRACT FROM AUTHOR]

Previous studies reported the inconsistent results on SPIKE, a quantitative trait locus, that controls the number of spikelets per panicle in rice. SPIKE increased grain yield under tropical conditions but did not increase it under temperate conditions. To reveal the effect of SPIKE on grain yield, we conducted an in-depth study of two varieties, IR64 and the near-isogenic line (NIL) for SPIKE in the IR64 genetic background, grown in research plots at the International Rice Research Institute in the tropics across 11 seasons from 2011 to 2017, and in 2018 with high and low nitrogen (N) fertilizer conditions, where mean yield variation was 417–670 g m−2. In multi-seasonal trials, overall yield performance of NIL-SPIKE was 11% superior to that of IR64. Significant variety × season interaction clarified NIL-SPIKE was superior to IR64 under the lower-yield seasons (< 500 g m−2) but the difference decreased or disappeared completely in the higher-yield seasons (> 500 g m−2). A subsequent N application trial with two levels of N fertilizer (45 and 180 kg N ha−1) confirmed a similar variety × N interaction for SPIKE; NIL-SPIKE tended to be superior to IR64 for grain yield under low-N application (431 g m−2), while the difference disappeared under high-N application (670 g m−2). The advantage of NIL-SPIKE under low-N application was due to more spikelets m−2 compared to IR64 but the difference disappeared under high-N application because there were fewer panicles m−2 in NIL-SPIKE compared to IR64. These results indicate SPIKE is effective for increasing rice yield under low-yield conditions (< 500 g m−2), namely low-N application or low soil fertility. Therefore, SPIKE should be used for breeding programs aimed at regions where soil fertility is poor or farmers cannot purchase adequate fertilizer. [ABSTRACT FROM AUTHOR]

The article discusses various reports within the issue about the progress in the human understanding on the nature and the roles of Fc receptors in diseases.