Dichotomy of Electronic Structure and Superconductivity between Single-Layer and Double-Layer FeSe/SrTiO3 Films

The latest discovery of possible high temperature superconductivity in the single-layer FeSe film grown on a SrTiO3 substrate, together with the observation of its unique electronic structure and nodeless superconducting gap, has generated much attention. Initial work also found that, while the single-layer FeSe/SrTiO3 film exhibits a clear signature of superconductivity, the double-layer FeSe/SrTiO3 film shows an insulating behavior. Such a dramatic difference between the single-layer and double-layer FeSe/SrTiO3 films is surprising and the underlying origin remains unclear. Here we report our comparative study between the single-layer and double-layer FeSe/SrTiO3 films by performing a systematic angle-resolved photoemission study on the samples annealed in vacuum. We find that, like the single-layer FeSe/SrTiO3 film, the as-prepared double-layer FeSe/SrTiO3 film is insulating and possibly magnetic, thus establishing a universal existence of the magnetic phase in the FeSe/SrTiO3 films. In particular, the double-layer FeSe/SrTiO3 film shows a quite different doping behavior from the single-layer film in that it is hard to get doped and remains in the insulating state under an extensive annealing condition. The difference originates from the much reduced doping efficiency in the bottom FeSe layer of the double-layer FeSe/SrTiO3 film from the FeSe-SrTiO3 interface. These observations provide key insights in understanding the origin of superconductivity and the doping mechanism in the FeSe/SrTiO3 films. The property disparity between the single-layer and double-layer FeSe/SrTiO3 films may facilitate to fabricate electronic devices by making superconducting and insulating components on the same substrate under the same condition.Comment: 19 pages, 4 figure

Hippo signalling governs cytosolic nucleic acid sensing through YAP/TAZ-mediated TBK1 blockade

The Hippo pathway senses cellular conditions and regulates YAP/TAZ to control cellular and tissue homeostasis, while TBK1 is central for cytosolic nucleic acid sensing and antiviral defence. The correlation between cellular nutrient/physical status and host antiviral defence is interesting but not well understood. Here we find that YAP/TAZ act as natural inhibitors of TBK1 and are vital for antiviral physiology. Independent of transcriptional regulation and through the transactivation domain, YAP/TAZ associate directly with TBK1 and abolish virus-induced TBK1 activation, by preventing TBK1 Lys63-linked ubiquitylation and the binding of adaptors/substrates. Accordingly, YAP/TAZ deletion/depletion or cellular conditions inactivating YAP/TAZ through Lats1/2 kinases relieve TBK1 suppression and boost antiviral responses, whereas expression of the transcriptionally inactive YAP dampens cytosolic RNA/DNA sensing and weakens the antiviral defence in cells and zebrafish. Thus, we describe a function of YAP/TAZ and the Hippo pathway in innate immunity, by linking cellular nutrient/physical status to antiviral host defence

Method for Evaluation and Application of Production Process Chain Complexity in Sewing Workshops considering Human Factor

Existing methods for evaluating manufacturing process chain complexity consider the number of machines, state of machines, number of parts, operation time, and processing sequence of parts. However, such evaluation methods ignore human factors. To consider human factors, human cognitive decision-making process factors are considered in the complexity evaluation of production processes. Accordingly, a new objective evaluation method of the human factor complexity is proposed. In the proposed method, sewing operations are taken as an example, and the human factor complexity is classified into perceived and cognitive complexity. Information entropy is used to measure cognitive complexity according to the type and quantity of sewing workers’ cognitive activities. The results show that various methods have significant differences in the evaluation of the complexity level of the production process chain. Specifically, the calculation results of the proposed evaluation method are much greater than those of other methods. This indicates that human cognitive and perceived complexities account for a large proportion. Therefore, human factor complexity cannot be omitted

Genome-wide identification and characterization of the Aquaporin gene family and transcriptional responses to boron deficiency in Brassica napus

Aquaporins (AQPs) are an abundant protein family and play important roles to facilitate small neutral molecule transport across membranes. Oilseed rape (Brassica napus L.) is an important oil crop in China and elsewhere in the world, and is very sensitive to low boron (B) stress. Several AQP family genes have been reported to be involved in B transport across plasma membranes in plants. In this study, a total of 121 full-length AQPs were identified and characterized in B. napus (AC genome), and could be classified into four sub-families, including 43 PIPs (plasma membrane intrinsic proteins), 35 TIPs (tonoplast intrinsic proteins), 32 NIPs (NOD26-like intrinsic proteins), and 11 SIPs (small basic intrinsic proteins). The gene characteristics of BnaAQPs were similar to those of BraAQPs (A genome) and BolAQPs (C genome) including the composition of each sub-family, gene structure, and substrate selectivity filters. The BnaNIP was the most complex AQP sub-family, reflecting the composition of substrate selectivity filter structures which affect the permeation of solution molecules. In this study, the seedlings of both B-efficient (QY10) and B-inefficient (W10) cultivars were treated with two boron (B) levels: deficient (0.25 μM B) and sufficient (25 μM B). The transcription of AQP genes in root (R), juvenile leaf (JL), and old leaf (OL) tissues of both cultivars was investigated under B deficient and sufficient conditions. Transcription of most BnaPIPs and BnaTIPs was significantly increased compared with other BnaAQPs in all the three tissues, especially in the roots, of both B-efficient and B-inefficient cultivars under both B conditions. With B deprivation, the expression of the majority of the BnaPIPs and BnaTIPs was down-regulated in the roots. However, the BnaNIPs were up-regulated. In addition, the BnaCnn_random.PIP1;4b, BnaPIP2;4s, BnaC04.TIP4;1a, BnaAnn_random.TIP1;1b, and BnaNIP5;1s (except for BnaA07.NIP5;1c and BnaC06.NIP5;1c) exhibited obvious differences at low B between B-efficient and B-inefficient cultivars. These results will help us to understand boron homeostasis in B. napus

Hippo signaling governs cytosolic nucleic acid sensing through YAP/TAZ-mediated TBK1 blockade

The Hippo pathway senses cellular conditions and regulates YAP/TAZ to control cellular and tissue homeostasis, while TBK1 is central for cytosolic nucleic acid sensing and antiviral defense. The correlation between cellular nutrient/physical status and host antiviral defense is interesting but not well understood. Here we find that YAP/TAZ act as natural inhibitors of TBK1 and are vital for antiviral physiology. Independent of transcriptional regulation and through transactivation domain, YAP/TAZ associate directly with TBK1 and abolish virus-induced TBK1 activation, by preventing TBK1 K63-linked ubiquitination and adaptors/substrates binding. Accordingly, YAP/TAZ deletion/depletion or cellular conditions inactivating YAP/TAZ through Lats1/2 kinases relieve TBK1 suppression and boost antiviral responses, whereas expression of the transcriptionally inactive YAP dampens cytosolic RNA/DNA sensing and weakens the antiviral defense in cells and zebrafish. Thus, we describe a function of YAP/TAZ and the Hippo pathway in innate immunity, by linking cellular nutrient/physical status to antiviral host defense

Hippo signalling governs cytosolic nucleic acid sensing through YAP/TAZ-mediated TBK1 blockade.

The Hippo pathway senses cellular conditions and regulates YAP/TAZ to control cellular and tissue homeostasis, while TBK1 is central for cytosolic nucleic acid sensing and antiviral defence. The correlation between cellular nutrient/physical status and host antiviral defence is interesting but not well understood. Here we find that YAP/TAZ act as natural inhibitors of TBK1 and are vital for antiviral physiology. Independent of transcriptional regulation and through the transactivation domain, YAP/TAZ associate directly with TBK1 and abolish virus-induced TBK1 activation, by preventing TBK1 Lys63-linked ubiquitylation and the binding of adaptors/substrates. Accordingly, YAP/TAZ deletion/depletion or cellular conditions inactivating YAP/TAZ through Lats1/2 kinases relieve TBK1 suppression and boost antiviral responses, whereas expression of the transcriptionally inactive YAP dampens cytosolic RNA/DNA sensing and weakens the antiviral defence in cells and zebrafish. Thus, we describe a function of YAP/TAZ and the Hippo pathway in innate immunity, by linking cellular nutrient/physical status to antiviral host defence

The protein phosphatase PPM1A dephosphorylates and activates YAP to govern mammalian intestinal and liver regeneration.

The Hippo-YAP pathway responds to diverse environmental cues to manage tissue homeostasis, organ regeneration, tumorigenesis, and immunity. However, how phosphatase(s) directly target Yes-associated protein (YAP) and determine its physiological activity are still inconclusive. Here, we utilized an unbiased phosphatome screening and identified protein phosphatase magnesium-dependent 1A (PPM1A/PP2Cα) as the bona fide and physiological YAP phosphatase. We found that PPM1A was associated with YAP/TAZ in both the cytoplasm and the nucleus to directly eliminate phospho-S127 on YAP, which conferring YAP the nuclear distribution and transcription potency. Accordingly, genetic ablation or depletion of PPM1A in cells, organoids, and mice elicited an enhanced YAP/TAZ cytoplasmic retention and resulted in the diminished cell proliferation, severe gut regeneration defects in colitis, and impeded liver regeneration upon injury. These regeneration defects in murine model were largely rescued via a genetic large tumor suppressor kinase 1 (LATS1) deficiency or the pharmacological inhibition of Hippo-YAP signaling. Therefore, we identify a physiological phosphatase of YAP/TAZ, describe its critical effects in YAP/TAZ cellular distribution, and demonstrate its physiological roles in mammalian organ regeneration