Significance Citrus bacterial canker, which is caused by several species in the genus Xanthomonas , is a severe disease with worldwide distribution affecting all the commercially important citrus species and cultivars. The mechanisms of canker development, involving erumpent pustule formation and bacterial growth, are not known. Our findings suggest that virulence determinants in several pathogens activate a single host disease susceptibility (S) gene that has a critical contribution to bacterial growth and host pustule development. The S gene represents an excellent candidate for control measures for the citrus bacterial canker.

Piezoelectric materials have been widely used for sensors, actuators, electronics, and energy conversion. Two-dimensional (2D) ultrathin semiconductors, such as monolayer h-BN and MoS with their atom-level geometry, are currently emerging as new and attractive members of the piezoelectric family. However, their piezoelectric polarization is commonly limited to the in-plane direction of odd-number ultrathin layers, largely restricting their application in integrated nanoelectromechanical systems. Recently, theoretical calculations have predicted the existence of out-of-plane and in-plane piezoelectricity in monolayer α-InSe. Here, we experimentally report the coexistence of out-of-plane and in-plane piezoelectricity in monolayer to bulk α-InSe, attributed to their noncentrosymmetry originating from the hexagonal stacking. Specifically, the corresponding d piezoelectric coefficient of α-InSe increases from 0.34 pm/V (monolayer) to 5.6 pm/V (bulk) without any odd-even effect. In addition, we also demonstrate a type of α-InSe-based flexible piezoelectric nanogenerator as an energy-harvesting cell and electronic skin. The out-of-plane and in-plane piezoelectricity in α-InSe flakes offers an opportunity to enable both directional and nondirectional piezoelectric devices to be applicable for self-powered systems and adaptive and strain-tunable electronics/optoelectronics.

Recent studies have indicated that the scavenger receptor class B type I (SR-BI) may play an important role in the uptake of high density lipoprotein (HDL) cholesteryl ester in liver and steroidogenic tissues. To investigate the in vivo effects of liver-specific SR-BI overexpression on lipid metabolism, we created several lines of SR-BI transgenic mice with an SR-BI genomic construct where the SR-BI promoter region had been replaced by the apolipoprotein (apo)A-I promoter. The effect of constitutively increased SR-BI expression on plasma HDL and non-HDL lipoproteins and apolipoproteins was characterized. There was an inverse correlation between SR-BI expression and apoA-I and HDL cholesterol levels in transgenic mice fed either mouse chow or a diet high in fat and cholesterol. An unexpected finding in the SR-BI transgenic mice was the dramatic impact of the SR-BI transgene on non-HDL cholesterol and apoB whose levels were also inversely correlated with SR-BI expression. Consistent with the decrease in plasma HDL and non-HDL cholesterol was an accelerated clearance of HDL, non-HDL, and their major associated apolipoproteins in the transgenics compared with control animals. These in vivo studies of the effect of SR-BI overexpression on plasma lipoproteins support the previously proposed hypothesis that SR-BI accelerates the metabolism of HDL and also highlight the capacity of this receptor to participate in the metabolism of non-HDL lipoproteins.The risk of developing coronary artery disease is directly related to plasma levels of low density lipoprotein (LDL) 1 cholesterol and inversely associated with the concentration of high density lipoprotein cholesterol (HDL) (1, 2). Although numerous studies have revealed many steps involved in LDL metabolism, significantly less is known about HDL metabolism. Novel insights concerning the metabolism of HDL have come from a recent series of experiments suggesting that the scavenger receptor class B type I (SR-BI) is an HDL receptor (3-9). SR-BI, a member of the CD36 superfamily, was originally cloned as a receptor for modified LDL (10 -12). Transfected cells expressing SR-BI show high affinity binding with HDL and take up cholesteryl ester from the particle by a selective uptake pathway markedly distinct from the LDL receptor pathway. Further support for SR-BI being an HDL receptor comes from the observations that SR-BI is expressed in liver and non-placental steroidogenic tissues, long hypothesized sites of HDL cholesterol delivery (3-6).The expression of SR-BI in tissues appears to be responsive to changes in hormonal status and HDL cholesteryl ester supply (13-16). In the adrenal glands of knockout mice deficient in apoA-I (13), hepatic lipase (13), or lecithin-cholesterol acyltransferase (14), the expression of SR-BI is increased markedly. Moreover, the expression of SR-BI is up-regulated in the adrenal gland and down-regulated in the liver of rats after high dose estrogen treatment (15). The estrogen-induced increase of SR-BI is accompanied by enhanced uptake of lipid ...

Key message A high-resolution genetic map combined with haplotype analyses identified a wheat ortholog of rice gene APO1 as the best candidate gene for a 7AL locus affecting spikelet number per spike. Abstract A better understanding of the genes controlling differences in wheat grain yield components can accelerate the improvements required to satisfy future food demands. In this study, we identified a promising candidate gene underlying a quantitative trait locus (QTL) on wheat chromosome arm 7AL regulating spikelet number per spike (SNS). We used large heterogeneous inbred families ( > 10,000 plants) from two crosses to map the 7AL QTL to an 87-kb region (674,019,191–674,106,327 bp, RefSeq v1.0) containing two complete and two partial genes. In this region, we found three major haplotypes that were designated as H1, H2 and H3. The H2 haplotype contributed the high-SNS allele in both H1 × H2 and H2 × H3 segregating populations. The ancestral H3 haplotype is frequent in wild emmer (48%) but rare (~ 1%) in cultivated wheats. By contrast, the H1 and H2 haplotypes became predominant in modern cultivated durum and common wheat, respectively. Among the four candidate genes, only TraesCS7A02G481600 showed a non-synonymous polymorphism that differentiated H2 from the other two haplotypes. This gene, designated here as WHEAT ORTHOLOG OF APO1 ( WAPO1 ), is an ortholog of the rice gene ABERRANT PANICLE ORGANIZATION 1 ( APO1 ), which affects spikelet number. Taken together, the high-resolution genetic map, the association between polymorphisms in the different mapping populations with differences in SNS, and the known role of orthologous genes in other grass species suggest that WAPO-A1 is the most likely candidate gene for the 7AL SNS QTL among the four genes identified in the candidate gene region. Electronic supplementary material The online version of this article (10.1007/s00122-019-03382-5) contains supplementary material, which is available to authorized users.

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Summary West Nile virus (WNV) causes an acute neurological infection attended by massive neuronal cell death. However, the mechanism(s) behind the virus-induced cell death is poorly understood. Using a library containing 77,406 sgRNAs targeting 20,121 genes, we performed a genome-wide screen followed by a second screen with a sub-library. Among the genes identified, seven genes, EMC2, EMC3, SEL1L, DERL2, UBE2G2, UBE2J1, and HRD1, stood out as having the strongest phenotype, whose knockout conferred strong protection against WNV-induced cell death with two different WNV strains and in three cell lines. Interestingly, knockout of these genes did not block WNV replication. Thus, these appear to be essential genes that link WNV replication to downstream cell death pathway(s). In addition, the fact that all of these genes belong to the endoplasmic reticulum-associated protein degradation (ERAD) pathway suggests that this might be the primary driver of WNV-induced cell death.

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