scholarly journals Comparison and Validation of Putative Pathogenicity-Related Genes Identified by T-DNA Insertional Mutagenesis and Microarray Expression Profiling inMagnaporthe oryzae

2017 ◽  
Vol 2017 ◽  
pp. 1-7
Author(s):  
Ying Wang ◽  
Ying Wáng ◽  
Qi Tan ◽  
Ying Nv Gao ◽  
Yan Li ◽  
...  

High-throughput technologies of functional genomics such as T-DNA insertional mutagenesis and microarray expression profiling have been employed to identify genes related to pathogenicity inMagnaporthe oryzae. However, validation of the functions of individual genes identified by these high-throughput approaches is laborious. In this study, we compared two published lists of genes putatively related to pathogenicity inM. oryzaeidentified by T-DNA insertional mutagenesis (comprising 1024 genes) and microarray expression profiling (comprising 236 genes), respectively, and then validated the functions of some overlapped genes between the two lists by knocking them out using the method of target gene replacement. Surprisingly, only 13 genes were overlapped between the two lists, and none of the four genes selected from the overlapped genes exhibited visible phenotypic changes on vegetative growth, asexual reproduction, and infection ability in their knockout mutants. Our results suggest that both of the lists might contain large proportions of unrelated genes to pathogenicity and therefore comparing the two gene lists is hardly helpful for the identification of genes that are more likely to be involved in pathogenicity as we initially expected.

2001 ◽  
Vol 12 (10) ◽  
pp. 758-764 ◽  
Author(s):  
Jonathan D. Choi ◽  
Lara A. Underkoffler ◽  
Joelle N. Collins ◽  
Shannon M. Marchegiani ◽  
Natalie A. Terry ◽  
...  

2004 ◽  
Vol 19 (3) ◽  
pp. 319-330 ◽  
Author(s):  
Harry Björkbacka ◽  
Katherine A. Fitzgerald ◽  
François Huet ◽  
Xiaoman Li ◽  
James A. Gregory ◽  
...  

Myeloid differentiation protein-88 (MyD88) is a signal adaptor protein required for cytokine production following engagement of Toll-like receptors (TLRs) by their cognate ligands. Activation of both TLR-3 and TLR-4, however, can engage signaling events independent of MyD88 expression. The relative importance of these MyD88-dependent and -independent signaling pathways in the macrophage response to lipopolysaccharide (LPS) is unknown. Here we define these events using microarray expression profiling of LPS-stimulated macrophages taken from MyD88-null and wild-type mice. Of the 1,055 genes found to be LPS responsive, only 21.5% were dependent on MyD88 expression, with MyD88-independent genes constituting 74.7% of the genetic response. This MyD88-independent gene expression was predominantly transcriptionally regulated, as it was unaffected by cycloheximide blockade of new protein synthesis. A previously undescribed group of LPS-regulated genes (3.8%), whose induction or repression was significantly greater in the absence of MyD88, was also identified by these studies. The regulation of these genes suggested that MyD88 could serve as a molecular brake, constraining gene activity in a subset of LPS-responsive genes. The findings generated with LPS stimulation were recapitulated by exposure of macrophages to live Escherichia coli. These expression-profiling studies redefine the current dogma of TLR-4 signaling and establish that MyD88, although essential for some of the best-characterized macrophage responses to LPS, is not required for the regulation of the majority of genes engaged by macrophage exposure to endotoxin or live bacteria.


2012 ◽  
Vol 5 (1) ◽  
pp. 232 ◽  
Author(s):  
Petra Kraus ◽  
Xing Xing ◽  
Siew Lim ◽  
Max E Fun ◽  
V Sivakamasundari ◽  
...  

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