bioRxiv Science⌕ Search

Biology subjects

Yang, S.-J.

Publications and source records attributed to Yang, S.-J..

5 recordsLinked to original sources

Bidirectional Energy Flow in the Photosystem II Supercomplex

The water splitting capability of Photosystem II (PSII) of plants and green algae requires the system to balance efficient light harvesting along with effective photoprotection against excitation in excess of photosynthetic capacity 1,2, particularly under the naturally fluctuating sunlight intensity. The comparatively flat energy landscape of the multi-component structure, inferred from spectra of the individual pigment-protein complexes and the rather narrow and featureless absorption spectrum, is well known 3-7. However, how the combination of the required functions emerge from the interactions among the multiple components of the PSII supercomplex (PSII-SC) cannot be inferred from the individual pigment-protein complexes. In this work, we investigate the energy transfer dynamics of the C2S2-type PSII-SC with a combined spectroscopic and modeling approach. Specifically, two-dimensional electronic-vibrational (2DEV) spectroscopy 8,9 provides enhanced spectral resolution and the ability to map energy evolution in real space, while the quantum dynamical simulation allows complete kinetic modeling of the 210 chromophores. We demonstrate that additional pathways emerge within the supercomplex. In particular, we show that excitation energy can leave the vicinity of the charge separation components, the reaction center (RC), faster than transferring to it. This enables activatable quenching centers in the periphery of the PSII-SC to be effective in removing excessive energy in cases of over-excitation 2. Overall, we provide a quantitative description of how the seemingly contradictory functions of PSII-SC arise from the combination of its individual components. This provides a fundamental understanding that will allow further improvement of artificial solar energy devices and bioengineering processes for increasing crop yield 10.

biophysics↗

Competitive asymmetry confers polyploid advantage under environmental stress

O_LICompetitive asymmetry across heterogeneous environments is crucial for the success of polyploid plants, however, little is known about it. As the major force in plant evolution, polyploids are predicted to maintain the competitive dominance relative to diploids under increased stress conditions. C_LIO_LITo evaluate the hypothesis of competitive asymmetry, we competed tetraploid and diploid plants of perennial herbaceous Chrysanthemum indicum L. (Asteraceae) at different relative frequencies under low and high water stress. We quantified the interaction intensity between competing plants of the same (intraploidy) and different ploidy levels (interploidy), and measured functional traits related to gas exchange and plant water use to understand the underlying mechanisms. C_LIO_LIStronger competitive effects of the tetraploid on diploid provided evidence for the competitive asymmetry between polyploid and diploid plants in C. indicum. Such competitive asymmetry was not only maintained under drought (increased water stress), but also translated into higher fitness of the tetraploid consistently across water stress conditions. Functional traits associated with fast growth and efficient water use likely explained the competitive dominance of the tetraploid. C_LIO_LIThese results will advance our understanding of species interactions between polyploid and diploid plants, and provide insights into population dynamics and species distribution under environmental change. C_LI

ecology↗

Unveiling the crucial role of type IV secretion system and motility of Helicobacter pylori in IL-1β production via NLRP3 inflammasome activation in neutrophils

Helicobacter pylori is a gram-negative, microaerophilic, and spiral-shaped bacterium and causes gastrointestinal diseases in human. IL-1{beta} is a representative cytokine produced in innate immune cells and is considered to be a key factor in the development of gastrointestinal malignancies. However, the mechanism of IL-1{beta} production by neutrophils during H. pylori infection is still unknown. We designed this study to identify host and bacterial factors involved in regulation of H. pylori-induced IL-1{beta} production in neutrophils. We found that H. pylori-induced IL-1{beta} production is abolished in NLRP3-, ASC-, and caspase-1/11-deficient neutrophils, suggesting essential role for NLRP3 inflammasome in IL-1{beta} response against H. pylori. Host TLR2, but not TLR4 and Nod2, was also required for transcription of NLRP3 and IL-1{beta} as well as secretion of IL-1{beta}. H. pylori lacking cagL, a key component of the type IV secretion system (T4SS), induced less IL-1{beta} production in neutrophils than did its isogenic WT strain, whereas vacA and ureA were dispensable. Moreover, T4SS was involved in caspase-1 activation and IL-1{beta} maturation in H. pylori-infected neutrophils. We also found that FlaA is essential for H. pylori-mediated IL-1{beta} production in neutrophils, but not dendritic cells. TLR5 and NLRC4 were not required for H. pylori-induced IL-1{beta} production in neutrophils. Instead, bacterial motility is essential for the production of IL-1{beta} in response to H. pylori. In conclusion, our study shows that host TLR2 and NLRP3 inflammasome and bacterial T4SS and motility are essential factors for IL-1{beta} production by neutrophils in response to H. pylori.\n\nIMPORTANCEIL-1{beta} is a representative pro-inflammatory cytokine and is considered to be a central host factor for the development of gastric cancers. Although neutrophils have been considered to be involved in H. pylori-induced gastric inflammation, the underlying mechanism by which H. pylori triggers IL-1{beta} production in neutrophils remains to be defined. In this study, our data suggested a critical role for the host TLR2 and NLRP3 inflammasome in IL-1{beta} production by neutrophil during H. pylori infection. Moreover, we found the bacterial factors, T4SS and FlaA, to be essential for IL-1{beta} production and NLRP3 activation during the course of H. pylori infection. Our current findings provide detailed molecular genetic mechanisms associated with IL-1{beta} production in neutrophils in response to H. pylori infection, which can serve as innovative anti-inflammatory targets to reduce H. pylori-induced gastric malignancies.

immunology↗

HBx enhances CPAP expression via interacting with CREB to promote hepatocarcinogenesis in HBV-associated HCC

Hepatitis B virus (HBV) encoded non-structure protein X (HBx) can promote cell proliferation, migration, and anti-apoptosis via activating several transcription factors and increasing their downstream gene expression in HBV-infected liver cells. Our previous report suggested that centrosomal P4.1-associated protein (CPAP) is required for HBx-mediated NF-{kappa}B activation. Here, we found that, upon HBV infection, overexpressed HBx can transcriptionally up-regulate CPAP via interacting with CREB. CPAP can directly interact with HBx to promote HBx-mediated cell proliferation and migration; and SUMO modification of CPAP is involved in interacting with HBx. Interestingly, CPAP can increase the HBx protein stability in an NF-{kappa}B-dependent manner; and overexpressed CPAP and HBx is positively correlated with the activation status of NF-{kappa}B in HCC. Increased expression of CREB and CPAP mRNAs exists in the high-risk group with a lower survival rate in hepatocellular carcinoma (HCC). These results suggest that the reciprocal regulation between CPAP and HBx may provide a microenvironment to facilitate HCC development via enhancing NF-{kappa}B activation, inflammatory cytokine production, and cancer maligancies. The findings of this study not only shed light on the role of CPAP in HBV-associated HCC, but also provide CPAP as a potential target for HBV-related HCC therapy.\n\nAuthor SummaryIn this study, we address a novel molecular mechanism for the collaboration between overexpressed HBx and CPAP in promoting hepatocarcinogenesis in HBV-associated HCC. Upon HBV infection, HBx is overexpressed and interacts with CREB to transcriptionally activate CPAP; the HBx/CPAP interaction promotes hepatocarcinogenesis. Clinical analysis found that co-overexpressed CPAP and CREB exist in the high-risk group with a lower survival rate in HCC. Additionally, overexpressed CPAP contributes to HBx protein stability in a NF-{kappa}B-dependent pathway. Our study provides a potential translational application in targeting CREB-CPAP axis in HBV-associated HCC.

cancer biology↗

Pericarp Pigmentation in ‘Red Delicious’ and Its Four Generation Mutants Correlates with Hormones

Bud sport mutants of apple (Malus domestica Borkh.) trees with a highly blushed colouring pattern are mainly caused by the accumulation of anthocyanins in the pericarp. Hormones are important factors modulating anthocyanin accumulation. However, a good understanding of the interplay between hormones and anthocyanin synthesis in apples, especially in mutants at the molecular level, remains elusive. Here, physiological and comparative transcriptome approaches were used to reveal the molecular basis of pericarp pigmentation in Red Delicious and its mutants, including Starking Red, Starkrimson, Campbell Redchief and Vallee spur, which were designated G0 to G4, respectively. Pericarp pigmentation gradually proliferated from G0 to G4. The anthocyanin content was higher in the mutants than in Red Delicious. The activation of early phenylpropanoid biosynthesis genes, including ASP3, PAL, 4CL, PER, CHS, CYP98A and F3H, was responsible for anthocyanin accumulation in mutants. In addition, IAA and ABA had a positive regulatory effect on the synthesis of anthocyanins, while GA had the reverse effect. The down-regulation of AACT1, HMGS, HMGR, MVK, MVD2, IDI1 and FPPS2 involved in terpenoid biosynthesis influences anthocyanin accumulation by positively regulating transcripts of AUX1 and SAUR that contribute to the synthesis of IAA, GID2 to GA, PP2C and SnRK2 to ABA. Furthermore, MYB and bHLH members, which are highly correlated (r=0.882-0.980) with anthocyanin content, modulated anthocyanin accumulation by regulating the transcription of structural genes, including CHS and F3H, involved in the flavonoid biosynthesis pathway.

bioinformatics↗