Genome-wide analysis of the nucleotide binding site leucine-rich repeat genes of four orchids revealed extremely low numbers of disease resistance genes

Orchids are one of the most diverse flowering plant families, yet possibly maintain the smallest number of the nucleotide-binding site-leucine-rich repeat (NBS-LRR) type plant resistance (R) genes among the angiosperms. In this study, a genome-wide search in four orchid taxa identified 186 NBS-LRR genes. Furthermore, 214 NBS-LRR genes were identified from seven orchid transcriptomes. A phylogenetic analysis recovered 30 ancestral lineages (29 CNL and one RNL), far fewer than other angiosperm families. From the genetics aspect, the relatively low number of ancestral R genes is unlikely to explain the low number of R genes in orchids alone, as historical gene loss and scarce gene duplication has continuously occurred, which also contributes to the low number of R genes. Due to recent sharp expansions, Phalaenopsis equestris and Dendrobium catenatum having 52 and 115 genes, respectively, and exhibited an "early shrinking to recent expanding" evolutionary pattern, while Gastrodia elata and Apostasia shenzhenica both exhibit a "consistently shrinking" evolutionary pattern and have retained only five and 14 NBS-LRR genes, respectively. RNL genes remain in extremely low numbers with only one or two copies per genome. Notably, all of the orchid RNL genes belong to the ADR1 lineage. A separate lineage, NRG1, was entirely absent and was likely lost in the common ancestor of all monocots. All of the TNL genes were absent as well, coincident with the RNL NRG1 lineage, which supports the previously proposed notion that a potential functional association between the TNL and RNL NRG1 genes

The reliability and validity of the Chinese version of Abbreviated PAD Emotion Scales

The study aimed at testing the reliabilityand validity of the Chinese version of Abbreviated PAD Emotion Scales using a Chinese sample. 297 Chinese undergraduate students were tested with the Chinese version of Abbreviated PAD Emotion Scales; 98 of them were retested with the same scales after seven days in order to assess thetest-retest reliability; and 102 of them were tested with SCL-90 at the same time which was intended as criteria for validity to assess the criterion validity. The results showedthat the Chinese version of Abbreviated PAD Emotion Scales displayed satisfying reliability and validity on P (pleasure-displeasure), only moderate reliability and validityon D (dominance-submissiveness), but quite low reliability and validity on A(arousal-nonarousal)The study aimed at testing the reliability and validity of the Chinese version of Abbreviated PAD Emotion Scales using a Chinese sample. 297 Chinese undergraduate students were tested with the Chinese version of Abbreviated PAD Emotion Scales; 98 of them were retested with the same scales after seven days in order to assess the test-retest reliability; and 102 of them were tested with SCL-90 at the same time which was intended as criteria for validity to assess the criterion validity. The results showed that the Chinese version of Abbreviated PAD Emotion Scales displayed satisfying reliability and validity on P (pleasure-displeasure), only moderate reliability and validity on D (dominance-submissiveness), but quite low reliability and validity on A (arousal-nonarousal)

Surfactant protein D modulates HIV infection of both T-cells and dendritic cells

Surfactant Protein D (SP-D) is an oligomerized C-type lectin molecule with immunomodulatory properties and involvement in lung surfactant homeostasis in the respiratory tract. SP-D binds to the enveloped viruses, influenza A virus and respiratory syncytial virus and inhibits their replication in vitro and in vivo. SP-D has been shown to bind to HIV via the HIV envelope protein gp120 and inhibit infectivity in vitro. Here we show that SP-D binds to different strains of HIV (BaL and IIIB) and the binding occurs at both pH 7.4 and 5.0 resembling physiological relevant pH values found in the body and the female urogenital tract, respectively. The binding of SP-D to HIV particles and gp120 was inhibited by the presence of several hexoses with mannose found to be the strongest inhibitor. Competition studies showed that soluble CD4 and CVN did not interfere with the interaction between SP-D and gp120. However, soluble recombinant DC-SIGN was shown to inhibit the binding between SP-D and gp120. SP-D agglutinated HIV and gp120 in a calcium dependent manner. SP-D inhibited the infectivity of HIV strains at both pH values of 7.4 and 5.0 in a concentration dependent manner. The inhibition of the infectivity was abolished by the presence of mannose. SP-D enhanced the binding of HIV to immature monocyte derived dendritic cells (iMDDCs) and was also found to enhance HIV capture and transfer to the T-cell like line PM1. These results suggest that SP-D can bind to and inhibit direct infection of T-cells by HIV but also enhance the transfer of infectious HIV particles from DCs to T-cells in vivo

Methylation matters: binding of Ets-1 to the demethylated Foxp3 gene contributes to the stabilization of Foxp3 expression in regulatory T cells

The forkhead-box protein P3 (Foxp3) is a key transcription factor for the development and suppressive activity of regulatory T cells (Tregs), a T cell subset critically involved in the maintenance of self-tolerance and prevention of over-shooting immune responses. However, the transcriptional regulation of Foxp3 expression remains incompletely understood. We have previously shown that epigenetic modifications in the CpG-rich Treg-specific demethylated region (TSDR) in the Foxp3 locus are associated with stable Foxp3 expression. We now demonstrate that the methylation state of the CpG motifs within the TSDR controls its transcriptional activity rather than a Treg-specific transcription factor network. By systematically mutating every CpG motif within the TSDR, we could identify four CpG motifs, which are critically determining the transcriptional activity of the TSDR and which serve as binding sites for essential transcription factors, such as CREB/ATF and NF-κB, which have previously been shown to bind to this element. The transcription factor Ets-1 was here identified as an additional molecular player that specifically binds to the TSDR in a demethylation-dependent manner in vitro. Disruption of the Ets-1 binding sites within the TSDR drastically reduced its transcriptional enhancer activity. In addition, we found Ets-1 bound to the demethylated TSDR in ex vivo isolated Tregs, but not to the methylated TSDR in conventional CD4+ T cells. We therefore propose that Ets-1 is part of a larger protein complex, which binds to the TSDR only in its demethylated state, thereby restricting stable Foxp3 expression to the Treg lineage

Differences in the Properties and Mirna Expression Profiles between Side Populations from Hepatic Cancer Cells and Normal Liver Cells

AIMS: Because hepatic cancer stem cells (HCSCs) are believed to derive from the conversion of hepatic normal stem cells (HNSCs), the identification of the differences that distinguish HCSCs from HNSCs is important. METHODS: The HCC model was established in F344 rats by DEN induction. Using FACS analysis, side population cells from HCC (SP-HCCs) were isolated from the epithelial-like cells of HCC tissues, and the side population cells from normal liver (SP-NLCs) were isolated from syngeneic normal liver cells. The expression of stem cell markers was detected in both freshly isolated and amplified subpopulations. After induction with HGF, the differentiation of each subpopulation was analyzed by detection of early and late liver markers. In vivo, the biological characteristics of SP-HCCs and SP-NLCs were analyzed by repairing injured livers or forming tumors in nude mice. In addition, the expression of miRNAs was examined in both populations by miRNA array and QRT-PCR. RESULTS: SP-NLCs and SP-HCCs were 4.30±0.011% and 2.100±0.010% of the whole population, respectively. Both SP-NLCs and SP-HCCs displayed greater expression of stem cell markers (CD133 and EpCAM) than NSP-NLCs and NSP-HCCs, respectively (P<0.01), both after fresh isolation and amplification. Upon HGF induction, SP-NLCs generated many ALB positive cells and few CK-7 positive cells, but NSP-NLCs could generate only ALB positive cells. In contrast, SP-HCCs gave rise to only AFP positive cells. As few as 5 × 10⁵ SP-NLCs were capable of repairing liver injury, while the same number of NSP-NLCs could not repair the liver. Furthermore, only 1 × 10⁴ SP-HCCs were necessary to initiate a tumor, while NSP-HCCs could not form a tumor. Compared to SP-NLCs, 68 up-regulated and 10 down-regulated miRNAs were present in SP-HCCs (P<0.01). CONCLUSION: Based on the decisive roles of some miRNAs in the genesis of HCSCs, miRNAs may contribute to the different characteristics that distinguish SP-HCCs from SP-NLCs

Atomic structure and defect dynamics of monolayer lead iodide nanodisks with epitaxial alignment on graphene

Lead Iodide (PbI2) is a large bandgap 2D layered material that has potential for semi- conductor applications. However, atomic level study of PbI2 monolayer has been limited due to challenges in obtaining thin crystals. Here, we use liquid exfoliation to produce monolayer PbI2 nanodisks (30-40 nm in diameter and > 99% monolayer purity) and deposit them onto suspended graphene supports to enable atomic structure study of PbI2. Strong epitaxial alignment of PbI2 monolayers with the underlying graphene lattice occurs, leading to a phase shift from the 1 T to 1 H structure to increase the level of commensuration in the two lattice spacings. The fundamental point vacancy and nanopore structures in PbI2 monolayers are directly imaged, showing rapid vacancy migration and self-healing. These results provide a detailed insight into the atomic structure of monolayer PbI2, and the impact of the strong van der Waals interaction with graphene, which has importance for future applications in optoelectronics

Platelet clearance via shear-induced unfolding of a membrane mechanoreceptor

Mechanisms by which blood cells sense shear stress are poorly characterized. In platelets, glycoprotein (GP)Ib-IX receptor complex has been long suggested to be a shear sensor and receptor. Recently, a relatively unstable and mechanosensitive domain in the GPIba subunit of GPIb-IX was identified. Here we show that binding of its ligand, von Willebrand factor, under physiological shear stress induces unfolding of this mechanosensory domain (MSD) on the platelet surface. The unfolded MSD, particularly the juxtamembrane € Trigger' sequence therein, leads to intracellular signalling and rapid platelet clearance. These results illustrate the initial molecular event underlying platelet shear sensing and provide a mechanism linking GPIb-IX to platelet clearance. Our results have implications on the mechanism of platelet activation, and on the pathophysiology of von Willebrand disease and related thrombocytopenic disorders. The mechanosensation via receptor unfolding may be applicable for many other cell adhesion receptors

Coronin-1A Links Cytoskeleton Dynamics to TCRαβ-Induced Cell Signaling

Actin polymerization plays a critical role in activated T lymphocytes both in regulating T cell receptor (TCR)-induced immunological synapse (IS) formation and signaling. Using gene targeting, we demonstrate that the hematopoietic specific, actin- and Arp2/3 complex-binding protein coronin-1A contributes to both processes. Coronin-1A-deficient mice specifically showed alterations in terminal development and the survival of αβT cells, together with defects in cell activation and cytokine production following TCR triggering. The mutant T cells further displayed excessive accumulation yet reduced dynamics of F-actin and the WASP-Arp2/3 machinery at the IS, correlating with extended cell-cell contact. Cell signaling was also affected with the basal activation of the stress kinases sAPK/JNK1/2; and deficits in TCR-induced Ca2+ influx and phosphorylation and degradation of the inhibitor of NF-κB (IκB). Coronin-1A therefore links cytoskeleton plasticity with the functioning of discrete TCR signaling components. This function may be required to adjust TCR responses to selecting ligands accounting in part for the homeostasis defect that impacts αβT cells in coronin-1A deficient mice, with the exclusion of other lympho/hematopoietic lineages