The effect of litter decomposition mostly depends on seasonal variation of ultraviolet radiation rather than species in a hyper-arid desert

Introduction: Ultraviolet (UV) radiation is believed to play a significant role in accelerating litter decomposition in water-limited ecosystems. Litter traits also influence the decomposition. However, the dominance of litter traits and ultraviolet radiation on litter decomposition in hyper-arid deserts (annual precipitation: potential evaporation < 0.05) with diverse species and seasonal variations remain unclear.Methods: To address this knowledge gap, we examined the decomposition of three dominant litter species (Karelinia caspia, Alhagi sparsifolia, and Populus euphratica) in the southern edge of the Taklimakan Desert, Northwest China.Results: Our results revealed that under UV radiation conditions, K. caspia, A. sparsifolia, and P. euphratica experienced mass losses of 45.4%, 39.8%, and 34.9%, respectively, and 20%, 22.2% and 17.4%, respectively under UV filtering treatment. Specifically, the loss rate of carbon and lignin under UV radiation, was 2.5 and 2.2 times higher than under UV filtering treatment, respectively.Conclusion: UV radiation did not dominate decomposition throughout the year in our study area, and the loss rate of litter traits was significantly higher in summer than in winter under UV radiation. Moreover, this photodegradation is related to the intensity of UV exposure, but not to precipitation or temperature. Surprisingly, species type had no significant effect on litter decomposition. However, when we applied a UV filtering treatment, we observed higher loss rates of nitrogen compared with the ambient treatment, suggesting the involvement of other spectra in the litter decomposition process. Overall, our findings elucidate that UV radiation is a crucial factor that affects litter mass loss. The magnitude of this effect mostly varies with the season rather than the species of litter

Integrated vs. sequential approaches for selecting and tuning CMA-ES variants

Algorithms and the Foundations of Software technolog

ChIP-seq and Functional Analysis of the SOX2 Gene in Colorectal Cancers

SOX2 is anHMGbox containing transcription factor that has been implicated in various types of cancer, but its role in colorectal cancers (CRC) has not been studied. Here we show that SOX2 is overexpressed in CRC tissues compared with normal adjacent tissues using immunohistochemical staining and RT-PCR. We also observed an increased SOX2 expression in nucleus of colorectal cancer tissues (46%, 14/30 cases vs. 7%, 2/30 adjacent tissues). Furthermore, knockdown of SOX2 in SW620 colorectal cancer cells decreased their growth rates in vitro cell line, and in vivo in xenograft models. ChIP-Seq analysis of SOX2 revealed a consensus sequence of wwTGywTT. An integrated expression profiling and ChIP-seq analysis show that SOX2 is involved in the BMP signaling pathway, steroid metabolic process, histone modifications, and many receptor-mediated signaling pathways such as IGF1R and ITPR2 (Inositol 1,4,5-triphosphate receptor, type 2).MOST, Chin

Acetylation Regulates Gluconeogenesis by Promoting PEPCK1 Degradation via Recruiting the UBR5 Ubiquitin Ligase

Protein acetylation has emerged as a major mechanism in regulating cellular metabolism. Whereas most glycolytic steps are reversible, the reaction catalyzed by pyruvate kinase is irreversible and the reverse reaction requires phosphoenolpyruvate carboxykinase (PEPCK1) to commit for gluconeogenesis. Here we show that acetylation regulates the stability of the gluconeogenic rate limiting enzyme PEPCK1, thereby modulating cellular response to glucose. High glucose destabilizes PEPCK1 by stimulating its acetylation. PEPCK1 is acetylated by the P300 acetyltransferase and this acetylation stimulates the interaction between PEPCK1 and UBR5, a HECT domain containing E3 ubiquitin ligase, therefore promoting PEPCK1 ubiquitinylation and degradation. Conversely, SIRT2 deacetylates and stabilizes PEPCK1. These observations represent an example that acetylation targets a metabolic enzyme to a specific E3 ligase in response to metabolic condition changes. Given that increased levels of PEPCK is linked with type II diabetes, this study also identifies potential therapeutic targets for diabetes

Comparing Arabidopsis receptor kinase and receptor protein-mediated immune signaling reveals BIK1-dependent differences

Pattern recognition receptors (PRRs) sense microbial patterns and activate innate immunity against attempted microbial invasions. The leucine‐rich repeat receptor kinases (LRR‐RK) FLS2 and EFR, and the LRR receptor protein (LRR‐RP) receptors RLP23 and RLP42, respectively, represent prototypical members of these two prominent and closely related PRR families. We conducted a survey of Arabidopsis thaliana immune signaling mediated by these receptors to address the question of commonalities and differences between LRR‐RK and LRR‐RP signaling. Quantitative differences in timing and amplitude were observed for several early immune responses, with RP‐mediated responses typically being slower and more prolonged than those mediated by RKs. Activation of RLP23, but not FLS2, induced the production of camalexin. Transcriptomic analysis revealed that RLP23‐regulated genes represent only a fraction of those genes differentially expressed upon FLS2 activation. Several positive and negative regulators of FLS2‐signaling play similar roles in RLP23 signaling. Intriguingly, the cytoplasmic receptor kinase BIK1, a positive regulator of RK signaling, acts as a negative regulator of RP‐type immune receptors in a manner dependent on BIK1 kinase activity. Our study unveiled unexpected differences in two closely related receptor systems and reports a new negative role of BIK1 in plant immunity

Flexible thermoelectric generator with high Seebeck coefficients made from polymer composites and heat-sink fabrics

Light and flexible thermoelectric generators working around room temperature and within a small temperature range are much desirable for numerous applications of wearable microelectronics, internet of things, and waste heat recovery. Herein, we report a high performance flexible thermoelectric generator made of polymeric thermoelectric composites and heat sink fabrics. The thermoelectric composites comprise n- and p-type Bi2Te3 particles and poly(3,4-ethylenedioxythiophene) polystyrene sulfonate, exhibiting a synergic effect that results in Seebeck coefficients higher than those of the constituent alloys and conductive polymer. The flexible and light thermoelectric generator produces an output power of 9.0 mW, a specific output power of 2.3 mW/g, and an areal power density of 6.5 W/m2 at ΔT = 45 K. By using the heat sink fabrics to maintain a large and uniform distribution of temperature difference across the generator, a three-fold increment of the output power is obtained

‘À La Carte’ Cyclic Hexapeptides: Fine Tuning Conformational Diversity while Preserving the Peptide Scaffold

Cyclic peptides have recently emerged as promising modulators of challenging protein‐protein interactions. Here we report on the design, synthesis and conformational behavior of a small library composed of C2 symmetric cyclic hexapeptides of type c(Xaa‐D‐Pro‐Yaa)2, where Xaa and Yaa are chosen from alanine, isoleucine, serine, glutamic acid, arginine and tryptophan due to the favorable properties of the side chains of these residues to recognize complex protein surfaces. We used a combination of nuclear magnetic resonance and molecular dynamic simulations to perform an extensive conformational analysis of a representative set of cyclic hexapeptides. Our results indicated that both the chemical nature and the chirality of the variable Xaa and Yaa positions play an important role in the cis/trans configuration of the Xaa‐D‐Pro bonds and in the conformational preferences of this family of peptides. This structural tuning can be exploited in design strategies seeking to optimize the binding efficiency and selectivity of cyclic hexapeptides towards protein surfaces

SIRT3-dependent GOT2 acetylation status affects the malate-aspartate NADH shuttle activity and pancreatic tumor growth

The malate–aspartate shuttle is indispensable for the net transfer of cytosolic NADH into mitochondria to maintain a high rate of glycolysis and to support rapid tumor cell growth. The malate–aspartate shuttle is operated by two pairs of enzymes that localize to the mitochondria and cytoplasm, glutamate oxaloacetate transaminases (GOT), and malate dehydrogenases (MDH). Here, we show that mitochondrial GOT2 is acetylated and that deacetylation depends on mitochondrial SIRT3. We have identified that acetylation occurs at three lysine residues, K159, K185, and K404 (3K), and enhances the association between GOT2 and MDH2. The GOT2 acetylation at these three residues promotes the net transfer of cytosolic NADH into mitochondria and changes the mitochondrial NADH/NAD+ redox state to support ATP production. Additionally, GOT2 3K acetylation stimulates NADPH production to suppress ROS and to protect cells from oxidative damage. Moreover, GOT2 3K acetylation promotes pancreatic cell proliferation and tumor growth in vivo. Finally, we show that GOT2 K159 acetylation is increased in human pancreatic tumors, which correlates with reduced SIRT3 expression. Our study uncovers a previously unknown mechanism by which GOT2 acetylation stimulates the malate–aspartate NADH shuttle activity and oxidative protection

The SOX2 response program in glioblastoma multiforme: an integrated ChIP-seq, expression microarray, and microRNA analysis

<p>Abstract</p> <p>Background</p> <p><it>SOX2 </it>is a key gene implicated in maintaining the stemness of embryonic and adult stem cells. <it>SOX2 </it>appears to re-activate in several human cancers including glioblastoma multiforme (GBM), however, the detailed response program of <it>SOX2 </it>in GBM has not yet been defined.</p> <p>Results</p> <p>We show that knockdown of the <it>SOX2 </it>gene in LN229 GBM cells reduces cell proliferation and colony formation. We then comprehensively characterize the <it>SOX2 </it>response program by an integrated analysis using several advanced genomic technologies including ChIP-seq, microarray profiling, and microRNA sequencing. Using ChIP-seq technology, we identified 4883 <it>SOX2 </it>binding regions in the GBM cancer genome. <it>SOX2 </it>binding regions contain the consensus sequence wwTGnwTw that occurred 3931 instances in 2312 <it>SOX2 </it>binding regions. Microarray analysis identified 489 genes whose expression altered in response to <it>SOX2 </it>knockdown. Interesting findings include that <it>SOX2 </it>regulates the expression of SOX family proteins <it>SOX1 </it>and <it>SOX18</it>, and that <it>SOX2 </it>down regulates <it>BEX1 </it>(brain expressed X-linked 1) and <it>BEX2 </it>(brain expressed X-linked 2), two genes with tumor suppressor activity in GBM. Using next generation sequencing, we identified 105 precursor microRNAs (corresponding to 95 mature miRNAs) regulated by <it>SOX2</it>, including down regulation of miR-143, -145, -253-5p and miR-452. We also show that miR-145 and <it>SOX2 </it>form a double negative feedback loop in GBM cells, potentially creating a bistable system in GBM cells.</p> <p>Conclusions</p> <p>We present an integrated dataset of ChIP-seq, expression microarrays and microRNA sequencing representing the <it>SOX2 </it>response program in LN229 GBM cells. The insights gained from our integrated analysis further our understanding of the potential actions of <it>SOX2 </it>in carcinogenesis and serves as a useful resource for the research community.</p

FTIP1 Is an Essential Regulator Required for Florigen Transport

FT-INTERACTING PROTEIN 1 is a novel protein that is involved in transporting florigen, a long-known mobile signal that induces flowering in plants in response to day length, from companion cells to sieve elements in the phloem of Arabidopsis