Engineered Cyanobacteria-Based Living Materials for Bioremediation of Heavy Metals Both In Vitro and In Vivo.

The pollution caused by heavy metals (HMs) represents a global concern due to their serious environmental threat. Photosynthetic cyanobacteria have a natural niche and the ability to remediate HMs such as cadmium. However, their practical application is hindered by a low tolerance to HMs and issues related to recycling. In response to these challenges, this study focuses on the development and evaluation of engineered cyanobacteria-based living materials for HMs bioremediation. Genes encoding phytochelatins (PCSs) and metallothioneins (MTs) were introduced into the model cyanobacterium Synechocystis sp. PCC 6803, creating PM/6803. The strain exhibited improved tolerance to multiple HMs and effectively removed a combination of Cd2+, Zn2+, and Cu2+. Using Cd2+ as a representative, PM/6803 achieved a bioremediation rate of approximately 21 µg of Cd2+/OD750 under the given test conditions. To facilitate its controllable application, PM/6803 was encapsulated using sodium alginate-based hydrogels (PM/6803@SA) to create "living materials" with different shapes. This system was feasible, biocompatible, and effective for removing Cd2+ under simulated conditions of zebrafish and mice models. Briefly, in vitro application of PM/6803@SA efficiently rescued zebrafish from polluted water containing Cd2+, while in vivo use of PM/6803@SA significantly decreased the Cd2+ content in mice bodies and restored their active behavior. The study offers feasible strategies for HMs bioremediation using the interesting biomaterials of engineered cyanobacteria both in vitro and in vivo.

Deficiency of Nuclear Receptor Coactivator 3 Aggravates Diabetic Kidney Disease by Impairing Podocyte Autophagy.

Nuclear receptors (NRs) are important transcriptional factors that mediate autophagy, preventing podocyte injury and the progression of diabetic kidney disease (DKD). However, the role of nuclear receptor coactivators that are powerful enhancers for the transcriptional activity of NRs in DKD remains unclear. In this study, a significant decrease in Nuclear Receptor Coactivator 3 (NCOA3) is observed in injured podocytes caused by high glucose treatment. Additionally, NCOA3 overexpression counteracts podocyte damage by improving autophagy. Further, Src family member, Fyn is identified to be the target of NCOA3 that mediates the podocyte autophagy process. Mechanistically, NCOA3 regulates the transcription of Fyn in a nuclear receptor, PPAR-γ dependent way. Podocyte-specific NCOA3 knockout aggravates albuminuria, glomerular sclerosis, podocyte injury, and autophagy in DKD mice. However, the Fyn inhibitor, AZD0530, rescues podocyte injury of NCOA3 knockout DKD mice. Renal NCOA3 overexpression with lentivirus can ameliorate podocyte damage and improve podocyte autophagy in DKD mice. Taken together, the findings highlight a novel target, NCOA3, that protects podocytes from high glucose injury by maintaining autophagy.

CPT1A Protects Podocytes From Lipotoxicity and Apoptosis In Vitro and Alleviates Diabetic Nephropathy In Vivo.

Defective fatty acid oxidation (FAO) has been implicated in diabetic kidney disease (DKD), yet little is known about the role of carnitine palmitoyltransferase-1A (CPT1A), a pivotal rate-limiting enzyme of FAO, in the progression of DKD. Here, we investigate whether CPT1A is a reliable therapeutic target for DKD. We first confirmed the downregulation expression of CPT1A in glomeruli from patients with diabetes. We further evaluated the function of CPT1A in diabetic models. Overexpression of CPT1A exhibited protective effects in diabetic conditions, improving albuminuria and glomerular sclerosis as well as mitigating glomerular lipid deposits and podocyte injury in streptozotocin-induced diabetic mice. Mechanistically, CPT1A not only fostered lipid consumption via fatty acid metabolism pathways, thereby reducing lipotoxicity, but also anchored Bcl2 to the mitochondrial membrane, thence preventing cytochrome C release and inhibiting the mitochondrial apoptotic process. Furthermore, a novel transcription factor of CPT1A, FOXA1, was identified. We elucidate the crucial role of CPT1A in mitigating podocyte injury and the progression of DKD, indicating that targeting CPT1A may be a promising avenue for DKD treatment.

Integrin ß8 prevents pericyte-myofibroblast transition and renal fibrosis through inhibiting the TGF-ß1/TGFBR1/Smad3 pathway in diabetic kidney disease.

Diabetic kidney disease (DKD) is one of the leading causes to develop end-stage kidney disease worldwide. Pericytes are implicated in the development of tissue fibrosis. However, the underlying mechanisms of pericytes in DKD remain largely unknown. We isolated and cultured primary pericytes and rat mesangial cells (HBZY-1). Western blot and qRT-PCR analysis were used to explore the role and regulatory mechanism of Integrin ß8/transforming growth factor beta 1 (TGF-ß1) pathway. We also constructed pericyte-specific Integrin ß8 knock-in mice as the research objects to determine the role of Integrin ß8 in vivo. We discovered that reduced Integrin ß8 expression was closely associated with pericyte transition in DKD. Overexpressed Integrin ß8 in pericytes dramatically suppressed TGF-ß1/TGF beta receptor 1 (TGFBR1)/Smad3 signaling pathway and protected glomerular endothelial cells (GECs) in vitro. In vivo, pericyte-specific Integrin ß8 knock-in ameliorated pericyte transition, endothelium injury and renal fibrosis in STZ-induced diabetic mice. Mechanistically, Murine double minute 2 (MDM2) was found to increase the degradation of Integrin ß8 and caused TGF-ß1 release and activation. Knockdown MDM2 could partly reverse the decline of Integrin ß8 and suppress pericytes transition. In conclusion, the present findings suggested that upregulated MDM2 expression contributes to the degradation of Integrin ß8 and activation of TGF-ß1/TGFBR1/Smad3 signaling pathway, which ultimately leads to pericyte transition during DKD progression. These results indicate MDM2/Integrin ß8 might be considered as therapeutic targets for DKD.

Asparagine endopeptidase protects podocytes in adriamycin-induced nephropathy by regulating actin dynamics through cleaving transgelin.

Focal segmental glomerulosclerosis (FSGS) is the most common glomerular disorder causing end-stage renal diseases worldwide. Central to the pathogenesis of FSGS is podocyte dysfunction, which is induced by diverse insults. However, the mechanism governing podocyte injury and repair remains largely unexplored. Asparagine endopeptidase (AEP), a lysosomal protease, regulates substrates by residue-specific cleavage or degradation. We identified the increased AEP expression in the primary proteinuria model which was induced by adriamycin (ADR) to mimic human FSGS. In vivo, global AEP knockout mice manifested increased injury-susceptibility of podocytes in ADR-induced nephropathy (ADRN). Podocyte-specific AEP knockout mice exhibited much more severe glomerular lesions and podocyte injury after ADR injection. In contrast, podocyte-specific augmentation of AEP in mice protected against ADRN. In vitro, knockdown and overexpression of AEP in human podocytes revealed the cytoprotection of AEP as a cytoskeleton regulator. Furthermore, transgelin, an actin-binding protein regulating actin dynamics, was cleaved by AEP, and, as a result, removed its actin-binding regulatory domain. The truncated transgelin regulated podocyte actin dynamics and repressed podocyte hypermotility, compared to the native full-length transgelin. Together, our data reveal a link between lysosomal protease AEP and podocyte cytoskeletal homeostasis, which suggests a potential therapeutic role for AEP in proteinuria disease.

Magnetic Field and Temperature-Dependent Brillouin Light Scattering Spectra of Magnons in Yttrium Iron Garnet.

Knowledge of the magnon responses to an external magnetic field and temperature is significant for spintronics applications. Herein, exploiting Brillouin light scattering (BLS) spectroscopy, we investigate the magnetic field and temperature dependence of the magnon frequency, line width, and intensity in yttrium iron garnet (YIG). The applied magnetic field here can effectively change the magnon frequency while maintaining the lifetime of the magnon. Specifically, we determine the temperature dependence of magnon frequency and the linear relationship between magneto-optic effects-related terms (|A(+)|2/|A(-)|2) and temperature below room temperature (RT), which can serve as a temperature sensor. Our results open an avenue to sense the temperature and the external magnetic field, including the effective magnetic field induced by the magnetic proximity effect. Furthermore, our results provide a route toward designing the operating frequency and loss of the devices, facilitating future research in spin-related applications, including magnon-based logic, memory, sensing, and thermospin devices.

Polymer-like Inorganic Double Helical van der Waals Semiconductor.

In high-performance flexible and stretchable electronic devices, conventional inorganic semiconductors made of rigid and brittle materials typically need to be configured into geometrically deformable formats and integrated with elastomeric substrates, which leads to challenges in scaling down device dimensions and complexities in device fabrication and integration. Here we report the extraordinary mechanical properties of the newly discovered inorganic double helical semiconductor tin indium phosphate. This spiral-shape double helical crystal shows the lowest Young's modulus (13.6 GPa) among all known stable inorganic materials. The large elastic (>27%) and plastic (>60%) bending strains are also observed and attributed to the easy slippage between neighboring double helices that are coupled through van der Waals interactions, leading to the high flexibility and deformability among known semiconducting materials. The results advance the fundamental understanding of the unique polymer-like mechanical properties and lay the foundation for their potential applications in flexible electronics and nanomechanics disciplines.

Conditional deletion of MAD2B in forebrain neurons enhances hippocampus-dependent learning and memory in mice.

Mitotic arrest deficient 2-like protein 2 (MAD2B) is not only a DNA damage repair agent but also a cell cycle regulator that is widely expressed in the hippocampus and the cerebral cortex. However, the functions of MAD2B in hippocampal and cerebral cortical neurons are poorly understood. In this study, we crossed MAD2B flox/flox and calcium/calmodulin-dependent protein kinase II alpha (Camk2a)-Cre mice to conditionally knock out MAD2B in the forebrain pyramidal neurons by the Cre/loxP recombinase system. First, RNA sequencing suggested that the differentially expressed genes in the hippocampus and the cerebral cortex between the WT and the MAD2B cKO mice were related to learning and memory. Then, the results of behavioral tests, including the Morris water maze test, the novel object recognition test, and the contextual fear conditioning experiment, suggested that the learning and memory abilities of the MAD2B cKO mice had improved. Moreover, conditional knockout of MAD2B increased the number of neurons without affecting the number of glial cells in the hippocampal CA1 and the cerebral cortex. At the same time, the number of doublecortin-positive (DCX+) cells was increased in the dentate gyrus (DG) of the MAD2B cKO mice. In addition, as shown by Golgi staining, the MAD2B cKO mice had more mushroom-like and long-like spines than the WT mice. Transmission electron microscopy (TEM) revealed that spine synapses increased and shaft synapses decreased in the CA1 of the MAD2B cKO mice. Taken together, our findings indicated that MAD2B plays an essential role in regulating learning and memory.

Regulation of Podocyte Injury by CircHIPK3/FUS Complex in Diabetic Kidney Disease.

Diabetic kidney disease (DKD) is a major microvascular complication of diabetes mellitus and is one of the leading causes of end-stage kidney disease. Circular RNAs (circRNAs) are a class of endogenous non-coding RNAs that play important roles in various diseases, yet their roles in DKD are poorly understood. CircRNA HIPK3 (circHIPK3), a highly conserved circRNA, is closely related to various cellular functions, including cell proliferation and apoptosis. The association between circHIPK3 and diabetic complications has been well demonstrated in multiple previous studies. However, the role of circHIPK3 in podocyte injury in DKD remains unclear. Herein, we discovered that circHIPK3 expression is markedly elevated in cultured podocytes under high-glucose (HG) conditions and glomeruli of diabetic mice, which is closely associated with podocyte injury in DKD. Functionally, lentivirus-mediated knockdown of circHIPK3 dramatically suppresses HG-induced podocyte apoptosis in vitro. Therapeutically, silencing circHIPK3 by adeno-associated virus-mediated RNA interference ameliorates podocyte injury and albuminuria in STZ-induced diabetic mice. Mechanistically, circHIPK3 facilitates the enrichment of fused in sarcoma (FUS) on the ectodysplasin A2 receptor (EDA2R) promoter, resulting in the upregulation of EDA2R expression and activation of apoptotic signaling. Taken together, these results indicate circHIPK3/FUS/EDA2R axis as a therapeutic target for podocyte injury and DKD progression.

Poly(maleic anhydride-alt-1-octadecene)-based bioadhesive nanovehicles improve oral bioavailability of poor water-soluble gefitinib.

The poor water solubility and inadequate oral bioavailability of gefitinib (Gef) remain a critical issue to achieve the therapeutic outcomes. Herein, we designed a poly(maleic anhydride-alt-1-octadecene) (PMA/C18) based lipid nanovehicle (PLN) to improve the intestinal absorption and oral bioavailability of poorly water-soluble Gef. PLN was nanometer-sized particles, and Gef was dispersed in the PLN formulation as amorphous or molecular state. At 4 h of oral administration, the tissue concentration of Gef in duodenum, jejunum, and ileum was profoundly enhanced 3.37-, 8.94-, and 8.09-fold by PLN when comparing to the counterpart lipid nanovehicle. Moreover, the oral bioavailability of Gef was significantly enhanced 2.48-fold by the PLN formulation when comparing to the free drug suspension. Therefore, this study provides an encouraging bioadhesive delivery platform to improve the oral delivery of poorly water-soluble drugs.

MAD2B promotes podocyte injury through regulating Numb-dependent Notch 1 pathway in diabetic nephropathy.

Rationale: Recent studies have demonstrated that the loss of podocyte is a critical event in diabetic nephropathy (DN). Previously, our group have found that the mitotic arrest deficient protein MAD2B was involved in high glucose (HG)-induced podocyte injury by regulating APC/C activity. However, the exact mechanism of MAD2B implicated in podocyte injury is still lacking. Methods: The experiments were conducted by using kidney tissues from streptozotocin (STZ) induced diabetic mice with or without podocyte-specific deletion of MAD2B and the cultured podocytes exposed to different treatments. Glomerular pathological injury was evaluated by periodic acid-Schiff staining and transmission electron microscopy. The endogenous interaction between MAD2B and Numb was discovered by yeast two-hybrid analysis and co-immunoprecipitation assay. The expressions of MAD2B, Numb and related pathway were detected by western blot, immunochemistry and immunofluorescence. Results: The present study revealed that MAD2B was upregulated in diabetic glomeruli and cultured podocytes under hyperglycemic conditions. Podocyte-specific deletion of MAD2B alleviated podocyte injury and renal function deterioration in mice of diabetic nephropathy. Afterwards, MAD2B was found to interact with Numb, which was downregulated in diabetic glomeruli and HG-stimulated cultured podocytes. Interestingly, MAD2B genetic deletion could partly reverse the decline of Numb in podocytes exposed to HG and in diabetic mice, and the expressions of Numb downstream molecules such as NICD and Hes-1 were decreased accordingly. In addition, overexpression of Numb ameliorated HG-induced podocyte injury. Conclusions: The present findings suggest that upregulated MAD2B expression contributes to Numb depletion and activation of Notch 1 signaling pathway, which ultimately leads to podocyte injury during DN progression.

Asparaginyl endopeptidase protects against podocyte injury in diabetic nephropathy through cleaving cofilin-1.

Podocyte injury and loss are critical events in diabetic nephropathy (DN); however, the underlying molecular mechanisms remain unclear. Here, we demonstrate that asparaginyl endopeptidase (AEP) protects against podocyte injury through modulating the dynamics of the cytoskeleton. AEP was highly upregulated in diabetic glomeruli and hyperglycemic stimuli treated-podocytes; however, AEP gene knockout and its compound inhibitor treatment accelerated DN in streptozotocin-induced diabetic mice, whereas specific induction of AEP in glomerular cells attenuated podocyte injury and renal function deterioration. In vitro, elevated AEP was involved in actin cytoskeleton maintenance and anti-apoptosis effects. Mechanistically, we found that AEP directly cleaved the actin-binding protein cofilin-1 after the asparagine 138 (N138) site. The protein levels of endogenous cofilin-1 1-138 fragments were upregulated in diabetic podocytes, consistent with the changes in AEP levels. Importantly, we found that cofilin-1 1-138 fragments were remarkably unphosphorylated than full-length cofilin-1, indicating the enhanced cytoskeleton maintenance activity of cofilin-1 1-138. Then we validated cofilin-1 1-138 could rescue podocytes from cytoskeleton disarrangement and injury in diabetic conditions. Taken together, our data suggest a protective role of elevated AEP in podocyte injury during DN progression through cleaving cofilin-1 to maintain podocyte cytoskeleton dynamics and defend damage.

Effects and mechanisms of probucol on aging-related hippocampus-dependent cognitive impairment.

BACKGROUND: In the present study, we aimed to investigate the effects of probucol on aging-related hippocampus-dependent cognitive impairment and explore the potential mechanisms. METHODS: D-galactose (100 mg/kg, once daily for 6 weeks) was subcutaneously injected to induce aging in mice. Then the mice were administered with probucol or vehicle once a day for 2 weeks. The hippocampus-related cognition was evaluated with Morris water maze test, novel object recognition test, and contextual fear conditioning test. Moreover, synaptic plasticity was assessed, and RNA-sequencing was applied to further explore the molecular mechanisms. RESULTS: Aging mice induced by D-galactose showed conspicuous learning and memory impairment, which was significantly ameliorated by probucol. Meanwhile, probucol enhanced the spine density and dendritic branches, improved long-term potentiation, and increased the expression of PSD95 of aging mice. Probucol regulated 70 differentially expressed genes compared to D-galactose group, of which 38 genes were upregulated and 32 genes were downregulated. At last, RNA-sequencing results were verified by quantitative reverse transcription-polymerase chain reaction. CONCLUSIONS: Probucol improved learning and memory in aging mice through enhancing synaptic plasticity and regulating gene expression, indicating the potential application of probucol to prevent and treat aging-related disorders.

Effects and Mechanisms of Synaptotagmin-7 in the Hippocampus on Cognitive Impairment in Aging Mice.

Aging is an irreversible biological process that involves oxidative stress, neuroinflammation, and apoptosis, and eventually leads to cognitive dysfunction. However, the underlying mechanisms are not fully understood. In this study, we investigated the role and potential mechanisms of Synaptotagmin-7, a calcium membrane transporter in cognitive impairment in aging mice. Our results indicated that Synaptotagmin-7 expression significantly decreased in the hippocampus of D-galactose-induced or naturally aging mice when compared with healthy controls, as detected by western blot and quantitative reverse transcriptase-polymerase chain reaction analysis. Synaptotagmin-7 overexpression in the dorsal CA1 of the hippocampus reversed long-term potentiation and improved hippocampus-dependent spatial learning in D-galactose-induced aging mice. Synaptotagmin-7 overexpression also led to fully preserved learning and memory in 6-month-old mice. Mechanistically, we demonstrated that Synaptotagmin-7 improved learning and memory by elevating the level of fEPSP and downregulating the expression of aging-related genes such as p53 and p16. The results of our study provide new insights into the role of Synaptotagmin-7 in improving neuronal function and overcoming memory impairment caused by aging, suggesting that Synaptotagmin-7 overexpression may be an innovative therapeutic strategy for treating cognitive impairment.

Deciphering and engineering photosynthetic cyanobacteria for heavy metal bioremediation.

Environmental pollution caused by heavy metals has received worldwide attentions due to their ubiquity, poor degradability and easy bioaccumulation in host cells. As one potential solution, photosynthetic cyanobacteria have been considered as promising remediation chassis and widely applied in various bioremediation processes of heavy-metals. Meanwhile, deciphering resistant mechanisms and constructing tolerant chassis towards heavy metals could greatly contribute to the successful application of the cyanobacteria-based bioremediation in the future. In this review, first we summarized recent application of cyanobacteria in heavy metals bioremediation using either live or dead cells. Second, resistant mechanisms and strategies for enhancing cyanobacterial bioremediation of heavy metals were discussed. Finally, potential challenges and perspectives for improving bioremediation of heavy metals by cyanobacteria were presented.

Effect of high intensity ultrasound on gelation properties of silver carp surimi with different salt contents.

Surimi from silver carp with different salt contents (0-5%) was obtained treated by high intensity ultrasound (HIU, 100 kHz 91 W·cm-2). The gelation properties of samples were evaluated by puncture properties, microstructures, water-holding capacity, dynamic rheological properties and intermolecular interactions. As the salt content increased from 0 to 5%, gel properties of surimi without HIU significantly improved. For samples with low-salt (0-2% NaCl) content, HIU induced obvious enhancement in breaking force and deformation. HIU promoted the protein aggregation linked by SS bonds, hydrophobic interactions and non-disulfide covalent bonds in surimi gels with low-salt content. Moreover, microstructures of HIU surimi gels with low-salt content were more compact than those of the corresponding control samples. HIU also improved the gelation properties of surimi with 3% NaCl to an extent. However, for high-salt (4-5% NaCl) samples, HIU decreased the breaking force and deformation of surimi gels due to the degradation of proteins suggested by increased TCA-soluble peptides. In conclusion, HIU effectively improved the gelation properties of surimi with low-salt content (0-2% NaCl), but was harmful for high-salt (4-5% NaCl) surimi. This might provide the theoretical basis for the production of low-salt surimi gels.

A transporter Slr1512 involved in bicarbonate and pH-dependent acclimation mechanism to high light stress in Synechocystis sp. PCC 6803.

High light (HL) exposure leads to photoinhibition and excess accumulation of toxic reactive oxygen species (ROS) in photosynthetic organisms, negatively impacting the global primary production. In this study, by screening a mutant library, a gene related with bicarbonate transport, slr1512, was found involved in HL acclimation in model cyanobacterium Synechocystis sp. PCC 6803. Comparative growth analysis showed that the slr1512 knockout mutant dramatically enhanced the tolerance of Synechocystis towards long-term HL stress (200 µmol photons m-2 s-1) than the wild type, achieving an enhanced growth by ~1.95-folds after 10 d. The phenotype differences between Δslr1512 and the wild type were analyzed via absorption spectrum and chlorophyll a content measurement. In addition, the accessible bicarbonate controlled by slr1512 and decreased PSII activity were demonstrated, and they were found to be the key factors affecting the tolerance of Synechocystis against HL stress. Further analysis confirmed that intracellular bicarbonate can significantly affect the activity of photosystem II, leading to the altered accumulation of toxic ROS under HL. Finally, a comparative transcriptomics was applied to determine the differential responses to HL between Δslr1512 and the wild type. This work provides useful insights to long-term acclimation mechanisms towards HL and valuable information to guide the future tolerance engineering of cyanobacteria against HL.

Improved Salt Tolerance and Metabolomics Analysis of Synechococcus elongatus UTEX 2973 by Overexpressing Mrp Antiporters.

The fast-growing cyanobacterium Synechococcus elongatus UTEX 2973 (Syn2973) is a promising candidate for photosynthetic microbial factory. Seawater utilization is necessary for large-scale cultivation of Syn2973 in the future. However, Syn2973 is sensitive to salt stress, making it necessary to improve its salt tolerance. In this study, 21 exogenous putative transporters were individually overexpressed in Syn2973 to evaluate their effects on salt tolerance. The results showed the overexpression of three Mrp antiporters significantly improved the salt tolerance of Syn2973. Notably, overexpressing the Mrp antiporter from Synechococcus sp. PCC 7002 improved cell growth by 57.7% under 0.4 M NaCl condition. In addition, the metabolomics and biomass composition analyses revealed the possible mechanisms against salt stress in both Syn2973 and the genetically engineered strain. The study provides important engineering strategies to improve salt tolerance of Syn2973 and is valuable for understanding mechanisms of salt tolerance in cyanobacteria.

Transporters Related to Stress Responses and Their Potential Application in Synechocystis sp. PCC 6803.

Cyanobacteria are autotrophic prokaryotes that can perform oxygenic photosynthesis. The conversion of light and carbon dioxide into green fuels and chemicals has drawn considerable interest, and several dozen products have been successfully synthesized in genetically engineered cyanobacteria. However, during cultivation, cyanobacterial cells are typically exposed to various stresses from the environment, such as acid, salt and metal stresses, as well as from the end products they synthesize, such as ethanol, butanol, and 3-hydroxypropionic acid (3-HP). These stresses hinder the accumulation of biomass and the production of chemicals or biofuels in cyanobacteria. Thus, improving the ability of cyanobacterial cells to resist stress can potentially enhance the robustness of the cyanobacterial chassis and the final yield of the target products. Toward this goal, research has been performed to explore the mechanisms by which cyanobacteria respond to various environmental perturbations and product toxicity. Among these mechanisms, transporters are membrane proteins involved in the transportation of ions, small molecules, or macromolecules across the membrane, and they have been reported to be involved in the response to common stresses in many organisms. Thus, engineering transporter-encoding genes may be a promising solution to increase the resistance of the cells against biotic and abiotic stresses. This chapter focuses on recent progress on the use of transporters related to stress responses in the model cyanobacterium Synechocystis sp. PCC 6803 and presents an updated review of their functions in stress regulation and their potential application in future chassis modifications.

Aggregation and conformational changes of silver carp myosin as affected by the ultrasound-calcium combination system.

BACKGROUND: Ultrasound and Ca2+ have been used separately to increase myosin properties in fish processing. However, little is know about how myosin changes are affected by Ca2+ and ultrasound in combination. The present study aimed to investigate the effects of the ultrasound-calcium combination system on aggregation and conformational changes of silver carp myosin. RESULTS: Ultrasound facilitated a Ca2+ -induced increase in turbidity. As the Ca2+ concentration increased from 0 to 100 mmol L-1 , there was an obvious increase in the turbidity, solubility and mean hydrated particle size of myosin after ultrasound treatment compared to without treatment. Moreover, changes of total and reactive SH contents depended on the ultrasound-calcium combination conditions. Under this combination system, myosin surface hydrophobicity significantly increased for the synergistic effect of ultrasound and Ca2+ . Furthermore, the ultrasound-calcium combination conditions could affect myosin gelation, with better gelation properties being observed for myosin treated with a combination of 60 mmol L-1 Ca2+ and 9 min of ultrasound. CONCLUSION: The combination system reported in the present study was beneficial for myosin unfolding, facilitating intermolecular interactions between Ca2+ and myosin. Ultrasound treatment promoted myosin aggregation via the induction of Ca2+ and reduced the critical concentration of Ca2+ required to aggregate myosin. In the fish processing industry, this combination system can enhance the gelation properties of surimi-based products. © 2018 Society of Chemical Industry.