Many plant cells respond to pathogens by the induction of phytoalexin biosynthesis, but the underlying changes of gene expression are often obscured by their close linkage to the complex rearrangements during pathogen...Many plant cells respond to pathogens by the induction of phytoalexin biosynthesis, but the underlying changes of gene expression are often obscured by their close linkage to the complex rearrangements during pathogen defense, especially the hypersensitive cell death. In root-derived cell cultures of Eschscholzia californica, the overproduction of cytotoxic benzophenanthridine alkaloids can be triggered by a minimum of pathogen pressure that does not evoke hypersensitive reactions. Such conditions activate a signal chain that is initiated by a short contact to low concentrations of yeast glycoprotein elicitor and includes a transient acidification of the cytoplasm. In contrast, high elicitor concentrations signal via an increase of jasmonate and trigger hypersensitive cell death, preceded by a drastic decay of translatable mRNAs. The main changes in protein and mRNA patterns caused by either signal path were compared by 2D proteomic separation, MS/MS sequencing and mRNA-in vitro translation. The four proteins showing the highest overexpression were identical between cells that received low or high-elicitor treatment and overlapped with the three proteins most upregulated by artificial pH shifts. They comprised one biosynthetic enzyme （norcoclaurine：SAM 4＇ O-methyl-transferase） plus a unique combination of stress-protective proteins： a heat shock protein （hsp 70）; a peptidyl-prolyl-cis/trans isomerase （cyclophilin）; and a glyceraldehyde-3-phosphate dehydrogenase. It appears that overproduction of the benzophenanthri- dine phytoalexins requires the up-regulation of a rate-limiting biosynthetic enzyme plus the coordinated expression of a specific set of protective enzymes and thus is managed like an oxidative stress.展开更多
Aging is one of the contributing risk factors for kidney diseases. Accumulating evidence prompts the view that telomere length in kidney tissue cells is an indicator for organismal aging. Previously identified aging m...Aging is one of the contributing risk factors for kidney diseases. Accumulating evidence prompts the view that telomere length in kidney tissue cells is an indicator for organismal aging. Previously identified aging markers （cathelin-related antimicrobial peptide （CRAMP）, stathmin, elongation factor-1α （EF-1α）, and chitinase） were associated not only with telomere driven aging in mice but also with human aging and chronic diseases. This study focuses on the relationship between these biomarkers and IgA nephropathy （IgAN） progression in the Chinese population. For 260 individuals, the four markers are determined in blind datasets using direct enzyme-linked immunosorbent assay （ELISA） and immunofluorescence staining. The expression levels of CRAMP and chitinase increased in blood plasma, urine, and kidney tissues during human IgAN progression. And for the other nephropathy, such as systemic lupus erythematosus （SLE）, diabetic nephropathy （DN）, and focal segmental glomerulosclerosis （FSGS）, there is no protein upregulaUon with telomere shortening. Moreover, a combination of CRAMP and chitinase can distinguish patients with IgAN from healthy individuals with 88.2%/92.5% （plasma） and 74.3%/84.2% （urine） sensitivity/specificity. These data provide the experimental evidence that telomere shortening and related inflammatory proteins are associated with human IgAN, and it could be a new direction for the disease progression study.展开更多
文摘Many plant cells respond to pathogens by the induction of phytoalexin biosynthesis, but the underlying changes of gene expression are often obscured by their close linkage to the complex rearrangements during pathogen defense, especially the hypersensitive cell death. In root-derived cell cultures of Eschscholzia californica, the overproduction of cytotoxic benzophenanthridine alkaloids can be triggered by a minimum of pathogen pressure that does not evoke hypersensitive reactions. Such conditions activate a signal chain that is initiated by a short contact to low concentrations of yeast glycoprotein elicitor and includes a transient acidification of the cytoplasm. In contrast, high elicitor concentrations signal via an increase of jasmonate and trigger hypersensitive cell death, preceded by a drastic decay of translatable mRNAs. The main changes in protein and mRNA patterns caused by either signal path were compared by 2D proteomic separation, MS/MS sequencing and mRNA-in vitro translation. The four proteins showing the highest overexpression were identical between cells that received low or high-elicitor treatment and overlapped with the three proteins most upregulated by artificial pH shifts. They comprised one biosynthetic enzyme （norcoclaurine：SAM 4＇ O-methyl-transferase） plus a unique combination of stress-protective proteins： a heat shock protein （hsp 70）; a peptidyl-prolyl-cis/trans isomerase （cyclophilin）; and a glyceraldehyde-3-phosphate dehydrogenase. It appears that overproduction of the benzophenanthri- dine phytoalexins requires the up-regulation of a rate-limiting biosynthetic enzyme plus the coordinated expression of a specific set of protective enzymes and thus is managed like an oxidative stress.
基金Project supported by the National Basic Research Program(973)of China(Nos.2011CB944002 and 2012CB517603)the National Natural Science Foundation of China(No.2011BAI10B07)the Major Special Project of Technology Office in Zhejiang Province(No.2012C13G2010133),China
文摘Aging is one of the contributing risk factors for kidney diseases. Accumulating evidence prompts the view that telomere length in kidney tissue cells is an indicator for organismal aging. Previously identified aging markers （cathelin-related antimicrobial peptide （CRAMP）, stathmin, elongation factor-1α （EF-1α）, and chitinase） were associated not only with telomere driven aging in mice but also with human aging and chronic diseases. This study focuses on the relationship between these biomarkers and IgA nephropathy （IgAN） progression in the Chinese population. For 260 individuals, the four markers are determined in blind datasets using direct enzyme-linked immunosorbent assay （ELISA） and immunofluorescence staining. The expression levels of CRAMP and chitinase increased in blood plasma, urine, and kidney tissues during human IgAN progression. And for the other nephropathy, such as systemic lupus erythematosus （SLE）, diabetic nephropathy （DN）, and focal segmental glomerulosclerosis （FSGS）, there is no protein upregulaUon with telomere shortening. Moreover, a combination of CRAMP and chitinase can distinguish patients with IgAN from healthy individuals with 88.2%/92.5% （plasma） and 74.3%/84.2% （urine） sensitivity/specificity. These data provide the experimental evidence that telomere shortening and related inflammatory proteins are associated with human IgAN, and it could be a new direction for the disease progression study.
