Comparative transcriptome analysis reveals the involvement of an MYB transcriptional activator, SmMYB108, in anther dehiscence in eggplant

Male sterility is a highly attractive agronomic trait as it effectively prevents self-fertilization and facilitates the production of high-quality hybrid seeds in plants. Timely release of mature pollen following anther dehiscence is essential for stamen development in flowering plants. Although several theories have been proposed regarding this, the specific mechanism of anther development in eggplant remains elusive. In this study, we selected an R2R3-MYB transcription factor gene, SmMYB108, that encodes a protein localized primarily in the nucleus by comparing the transcriptomics of different floral bud developmental stages of the eggplant fertile line, F142. Quantitative reverse transcription polymerase chain reaction revealed that SmMYB108 was preferentially expressed in flowers, and its expression increased significantly on the day of flowering. Overexpression of SmMYB108 in tobacco caused anther dehiscence. In addition, we found that SmMYB108 primarily functions as a transcriptional activator via C-terminal activation (amino acid 262–317). Yeast one-hybrid and dual-luciferase reporter assays revealed that genes (SmMYB21, SmARF6, and SmARF8) related to anther development targeted the SmMYB108 promoter. Overall, our results provide insights into the molecular mechanisms involved in the regulation of anther development by SmMYB108

Chemical approaches to cell reprogramming

Recent advances in cell reprogramming via employing different sets of factors, which allows generation of various cell types that are beyond the downstream developmental lineages from the starting cell type, provide significant opportunities to study fundamental biology and hold enormous promise in regenerative medicine. Small molecules have been identified to enhance and enable reprogramming by regulating various mechanisms, and provide a highly temporal and tunable approach to modulate cellular fate and functions. Here, we review the latest development in cell reprogramming from the perspective of small molecule modulation

SNX27-driven membrane localisation of OTULIN antagonises linear ubiquitination and NF-kappa B signalling activation

BACKGROUND: Linear ubiquitination is a novel type of ubiquitination that plays important physiological roles in signalling pathways such as tumour necrosis factor (TNF) signalling. However, little is known about the regulatory mechanisms of linear ubiquitination, except the well-described enzymatic regulators E3 ligase linear ubiquitin chain assembly complex (LUBAC) and deubiquitinase OTULIN. RESULTS: Previously, we identified SNX27, a member of the sorting nexin family protein, as a selective linear ubiquitin chain interactor in mass spectrometry-based ubiquitin interaction screening. Here, we demonstrated that the interaction between the linear ubiquitin chain and SNX27 is mediated by the OTULIN. Furthermore, we found that SNX27 inhibits LUBAC-mediated linear ubiquitin chain formation and TNFα-induced signalling activation. Mechanistic studies showed that, upon TNFα stimulation, OTULIN-SNX27 is localised to membrane-associated TNF receptor complex, where OTULIN deubiquitinates the linear polyubiquitin chain that formed by the LUBAC complex. Significantly, chemical inhibition of SNX27-retromer translocation by cholera toxin inhibits OTULIN membrane localization. CONCLUSIONS: In conclusion, our study demonstrated that SNX27 inhibits TNFα induced NF-κB signalling activation via facilitating OTULIN to localize to TNF receptor complex. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13578-021-00659-5

Small molecules targeting ROR gamma t inhibit autoimmune disease by suppressing Th17 cell differentiation

Th17 cells, a lymphocyte subpopulation that is characterized by the expression of the transcription factor "retinoic acid receptor-related orphan receptor gamma-t" (ROR gamma t), plays an important role in the pathogenesis of autoimmune disease. The current study was set up to discover novel and non-steroidal small-molecule inverse agonists of ROR gamma t and to determine their effects on autoimmune disease. Structure-based virtual screening (SBVS) was used to find compounds targeting ROR gamma t. Flow cytometry was used to detect the Th17 cell differentiation. Inverse agonists were intraperitoneally administered to mice undergoing experimental autoimmune uveitis (EAU), experimental autoimmune encephalomyelitis (EAE) or type 1 diabetes. The effects of the inverse agonists were evaluated by clinical or histopathological scoring. Among 1.3 million compounds screened, CQMU151 and CQMU152 were found to inhibit Th17 cell differentiation without affecting the differentiation of Th1 and Treg lineages (bothP = 0.001). These compounds also reduced the severity of EAU (P = 0.01 and 0.013) and functional studies showed that they reduced the number of Th17 cell and the expression of IL-17(Th17), but not IFN-gamma(Th1) and TGF-beta(Treg) in mouse retinas. Further studies showed that these compounds may reduce the expression of p-STAT3 by reducing the positive feedback loop of IL-17/IL-6/STAT3. These compounds also reduced the impaired blood-retinal barrier function by upregulating the expression of tight junction proteins. These compounds were also found to reduce the severity of EAE and type 1 diabetes. Our results showed that ROR gamma t inverse agonists may inhibit the development of autoimmune diseases and may provide new clues for the treatment of Th17-mediated immune diseases

The preparation of a bio-polyelectrolytes based core-shell structure and its application in flame retardant polylactic acid composites

A bio-polyelectrolyte (PC) was synthesized by reacting phytic acid (PA) with casein (CS), and used as the shell materials to microencapsulate ammonium polyphosphate (APP). The obtained core-shell structured flame retardant (PC@APP) was incorporated into polylactic acid (PLA). The dispersion of PC@APP was greatly improved. As a result, the elongation at break and notched impact strength were improved from 6.9% and 3.5 KJ/m2 of neat PLA sample to 14.4% and 4.7 KJ/m2 of PLA samples containing 5%PC@APP. Moreover, the fire resistance of PLA/5%PC@APP composites was also enhanced. The limiting oxygen index (LOI) value was increased from 19.6% to 28.3%; the vertical burning (UL-94) rating was upgraded from no rating to V-0; and the peak heat release rate value was decreased from 935.8 kW/m2 to 747.9 kW/m2. It is suggested that the well-dispersed PC@APP alters the degradation routine of PLA matrix, leading to the rapid formation of physical barriers

Mapping protein direct interactome of oxidoreductases with small molecular chemical cross-linkers in live cells

Identifying direct substrates of enzymes has been a long-term challenge. Here, we present a strategy using live cell chemical cross-linking and mass spectrometry to identify the putative substrates of enzymes for further biochemical validation. Compared with other methods, our strategy is based on the identification of cross-linked peptides supported by high-quality MS/MS spectra, which eliminates false-positive discoveries of indirect binders. Additionally, cross-linking sites allow the analysis of interaction interfaces, providing further information for substrate validation. We demonstrated this strategy by identifying direct substrates of thioredoxin in both E. coli and HEK293T cells using two bis-vinyl sulfone chemical cross-linkers BVSB and PDES. We confirmed that BVSB and PDES have high specificity in cross-linking the active site of thioredoxin with its substrates both in vitro and in live cells. Applying live cell cross-linking, we identified 212 putative substrates of thioredoxin in E. coli and 299 putative S-nitrosylation (SNO) substrates of thioredoxin in HEK293T cells. In addition to thioredoxin, we have shown that this strategy can be applied to other proteins in the thioredoxin superfamily. Based on these results, we believe future development of cross-linking techniques will further advance cross-linking mass spectrometry in identifying substrates of other classes of enzymes

The Effect of Additive Ce￣(4+) on the Properties of composite coating of Co-P-PTFE

探讨了添加剂Ｃｅ~（４＋）对Ｃｏ－Ｐ－ＰＴＦＥ复合镀层的影响，结果表明，添加剂Ｃｅ~（４＋）可降低Ｃｏ－Ｐ－ＰＴＦＥ复合镀层在３％ＮａＣｌ溶液中的腐蚀电流，提高其耐蚀性。同时使复合镀层微观结构发生变化，择优取向由（１００）面转变为（１１０）面，且晶粒尺寸降低．The effect of additive Ce4+ on the properties of composite coating of Co-P-PTFE was studied in this paper.The results show that additive Ce(4+) can change the structures and properties of Co-P-PTFE composite coating. First,the surface of the compoite coating becomes smooth and the microhardness of the composite coating increased.Secondly,additive Ce(4+) decreased the corrosion current lcorr of the composite coating in the solution of 3% NaCl and increased its property of anticorrosion.Finally additive Ce(4+) can affect preferred orientation and grain size of composite coating of Co-P-PTFE. Preferred orientation of the composite varies from(100)to(110)and the grain size decreased.作者联系地址：厦门大学化学系Author's Address: Chemistry Department,Xiamen University,Xiamen,36100