Anti-TM9SF2 (aa 116-215) polyclonal antibody

Tapping panel dryness (TPD) causes a significant reduction in the latex yield of rubber tree (Hevea brasiliensis Muell. Arg.). It is reported that TPD is a typical programmed cell death (PCD) process. Although PCD plays a vital role in TPD occurrence, there is a lack of detailed and systematic study. Metacaspases are key regulators of diverse PCD in plants. Based on our previous result that HbMC1 was associated with TPD, we further elucidate the roles of HbMC1 on rubber tree TPD in this study. HbMC1 was up-regulated by TPD-inducing factors including wounding, ethephon and H2O2. Moreover, the expression level of HbMC1 was increased along with TPD severity in rubber tree, suggesting a positive correlation between HbMC1 expression and TPD severity. To investigate its biological function, HbMC1 was overexpressed in yeast (Saccharomyces cerevisiae) and tobacco (Nicotiana benthamiana). Transgenic yeast and tobacco overexpressing HbMC1 showed growth retardation compared with controls under H2O2-induced oxidative stress. In addition, overexpression of HbMC1 in yeast and tobacco reduced cell survival after high-concentration H2O2 treatment and resulted in enhanced H2O2-induced leaf cell death, respectively. A total of 11 proteins, rbcL, TM9SF2-like, COX3, ATP9, DRP, HbREF/Hevb1, MSSP2-like, SRC2, GATL8, CIPK14-like and STK, were identified and confirmed to interact with HbMC1 by yeast two-hybrid screening and co-transformation in yeast. The 11 proteins mentioned above are associated with many biological processes, including rubber biosynthesis, stress response, autophagy, carbohydrate metabolism, signal transduction, etc. Taken together, our results suggest that HbMC1-mediated PCD plays an important role in rubber tree TPD, and the identified HbMC1-interacting proteins provide valuable information for further understanding the molecular mechanism of HbMC1-mediated TPD in rubber tree.

Genome-wide association studies (GWAS) of chronic periodontitis (CP) defined by clinical criteria alone have had modest success to-date. Here, we refine the CP phenotype by supplementing clinical data with biological intermediates of microbial burden (levels of eight periodontal pathogens) and local inflammatory response (gingival crevicular fluid IL-1 beta) and derive periodontal complex traits (PCTs) via principal component analysis. PCTs were carried forward to GWAS (similar to 2.5 million markers) to identify PCT-associated loci among 975 European American adult participants of the Dental ARIC study. We sought to validate these findings for CP in the larger ARIC cohort (n = 821 participants with severe CP, 2031-moderate CP, 1914-healthy/mild disease) and an independent German sample including 717 aggressive periodontitis cases and 4210 controls. We identified six PCTs with distinct microbial community/IL-1 beta structures, although with overlapping clinical presentations. PCT1 was characterized by a uniformly high pathogen load, whereas PCT3 and PCT5 were dominated by Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, respectively. We detected genome-wide significant signals for PCT1 (CLEC19A, TRA, GGTA2P, TM9SF2, IFI16, RBMS3), PCT4 (HPVC1) and PCT5 (SLC15A4, PKP2, SNRPN). Overall, the highlighted loci included genes associated with immune response and epithelial barrier function. With the exception of associations of BEGAIN with severe and UBE3D with moderate CP, no other loci were associated with CP in ARIC or aggressive periodontitis in the German sample. Although not associated with current clinically determined periodontal disease taxonomies, upon replication and mechanistic validation these candidate loci may highlight dysbiotic microbial community structures and altered inflammatory/immune responses underlying biological sub-types of CP.