scholarly journals Bemisia tabaci-infested tomato plants show phase-specific pattern of photosynthetic gene expression indicative of disrupted electron flow leading to photo-oxidation and plant death

2009 ◽  
Vol 4 (10) ◽  
pp. 992-995
Author(s):  
John Paul Délano-Frier ◽  
María Gloria Estrada-Hernández
2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Diego Guerrieri ◽  
Luis Re ◽  
Jorgelina Petroni ◽  
Nella Ambrosi ◽  
Roxana E. Pilotti ◽  
...  

Background.Delayed graft function (DGF) remains an important problem after kidney transplantation and reduced long-term graft survival of the transplanted organ. The aim of the present study was to determine if the development of DGF was associated with a specific pattern of inflammatory gene expression in expanded criteria of deceased donor kidney transplantation. Also, we explored the presence of correlations between DGF risk factors and the profile that was found.Methods.Seven days after kidney transplant, a cDNA microarray was performed on biopsies of graft from patients with and without DGF. Data was confirmed by real-time PCR. Correlations were performed between inflammatory gene expression and clinical risk factors.Results.From a total of 84 genes analyzed, 58 genes were upregulated while only 1 gene was downregulated in patients with DGF compared with no DGF (P=0.01). The most relevant genes fold changes observed was IFNA1, IL-10, IL-1F7, IL-1R1, HMOX-1, and TGF-β. The results were confirmed for IFNA1, IL-1R1, HMOX-1 and TGF-β. A correlation was observed between TGF-β, donor age, and preablation creatinine, but not body mass index (BMI). Also, TGF-βshowed an association with recipient age, while IFNA1 correlated with recipient BMI. Furthermore, TGF-β, IFNA1 and HMOX-1 correlated with several posttransplant kidney function markers, such as diuresis, ultrasound Doppler, and glycemia.Conclusions.Overall, the present study shows that DGF is associated with inflammatory markers, which are correlated with donor and recipient DGF risk factors.


2004 ◽  
Vol 562 (1) ◽  
pp. 223-234 ◽  
Author(s):  
Céline Marionneau ◽  
Brigitte Couette ◽  
Jie Liu ◽  
Huiyu Li ◽  
Matteo E. Mangoni ◽  
...  

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Sarah Franklin ◽  
Haodong Chen ◽  
Scherise Mitchell-Jordan ◽  
Shuxun Ren ◽  
Peipei Ping ◽  
...  

Nuclear DNA is packaged around the octameric nucleosome core particle, constituting the basic building block of chromatin. Non-nucleosome chromatin structural molecules have been shown to induce higher order packaging of DNA into structurally compact and inactive heterochromatin, or loosely packed and active euchromatin. These chromatin remodeling events are thought to establish a cell type specific pattern of gene expression. During the development of cardiac hypertrophy and failure, genes normally only expressed during development are re-activated. While a number of transcription factors involved in these changes in fetal gene expression have been identified, the means for genome-wide structural remodeling of DNA are unknown. To identify factors controlling genomic plasticity in cardiomyocytes, we used mass spectrometry to quantify chromatin-associated proteins from cardiac nuclei during stages of hypertrophy and failure in the mouse. Adult mice were subjected to cardiac pressure overload by transverse aortic constriction. Chromatin was fractionated from cardiac nuclei and DNA-bound proteins were acid extracted and analyzed by mass spectrometry. We measured chromatin occupancy patterns for >300 proteins during distinct stages of heart failure. To explore the isoform specific roles of individual chromatin structural proteins, we used siRNA to knock-down expression of two high mobility group proteins (HMGB1 and 2) exhibiting altered expression in the hypertrophic heart. Loss of HMGB2 (but not HMGB1) induced robust hypertrophic growth in cardiomyocytes. qRT-PCR analyses demonstrated that HMGB2 is responsible for some but not all changes in the fetal gene program (ANF increased 150% and SERCA decreased 20%, whereas α- and β-MHC were unchanged). To further explore the endogenous regions of the genome under control of HMGB2 packing, we performed microarrays following HMGB2 knockdown. Hypertrophy or HMGB2 knock-down induced global chromatin remodeling conducive to gene expression, as measured by histone post-translational modifications and the ratio of core to linker histones. These studies reveal a novel role of HMGB2 to inhibit hypertrophic growth and provide insights into general principles for genome-wide chromatin remodeling.


Development ◽  
1998 ◽  
Vol 125 (13) ◽  
pp. 2511-2520 ◽  
Author(s):  
S. Fujiwara ◽  
J.C. Corbo ◽  
M. Levine

Previous studies have identified a minimal 434 bp enhancer from the promoter region of the Ciona Brachyury gene (Ci-Bra), which is sufficient to direct a notochord-specific pattern of gene expression. Here we present evidence that a Ciona homolog of snail (Ci-sna) encodes a repressor of the Ci-Bra enhancer in the tail muscles. DNA-binding assays identified four Ci-Sna-binding sites in the Ci-Bra enhancer, and mutations in these sites cause otherwise normal Ci-Bra/lacZ transgenes to be misexpressed in ectopic tissues, particularly the tail muscles. Selective misexpression of Ci-sna using a heterologous promoter results in the repression of Ci-Bra/lacZ transgenes in the notochord. Moreover, the conversion of the Ci-Sna repressor into an activator results in the ectopic induction of Ci-Bra/lacZ transgenes in the muscles, and also causes an intermixing of notochord and muscle cells during tail morphogenesis. These results suggest that Ci-Sna functions as a boundary repressor, which subdivides the mesoderm into separate notochord and tail muscle lineages.


2020 ◽  
Vol 11 ◽  
Author(s):  
Maria Tartaglia ◽  
Simona Arena ◽  
Andrea Scaloni ◽  
Mauro Marra ◽  
Mariapina Rocco

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