Development of a high throughput transformation system for insertional mutagenesis in Magnaporthe oryzae

2007 ◽  
Vol 44 (10) ◽  
pp. 1035-1049 ◽  
Author(s):  
Melania F. Betts ◽  
Sara L. Tucker ◽  
Natalia Galadima ◽  
Yan Meng ◽  
Gayatri Patel ◽  
...  
Author(s):  
Christian Südfeld ◽  
Michal Hubáček ◽  
Daniel Rodrigues Figueiredo ◽  
Mihris I.S. Naduthodi ◽  
John van der Oost ◽  
...  

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Shigeo S. Sugano ◽  
Hiroko Suzuki ◽  
Eisuke Shimokita ◽  
Hirofumi Chiba ◽  
Sumihare Noji ◽  
...  

2008 ◽  
Vol 21 (5) ◽  
pp. 525-534 ◽  
Author(s):  
Junhyun Jeon ◽  
Jaeduk Goh ◽  
Sungyong Yoo ◽  
Myoung-Hwan Chi ◽  
Jaehyuk Choi ◽  
...  

Insertional mutagenesis of Magnaporthe oryzae led to the identification of MCK1, a pathogenicity gene predicted to encode mitogen-activated protein kinase kinase kinase (MAPKKK) homologous to BCK1 in Saccharomyces cerevisiae. Targeted disruption of MCK1 resulted in the fungus undergoing autolysis and showing hypersensitivity to cell-wall-degrading enzyme. The mck1 produced significantly reduced numbers of conidia and developed appressoria in a slightly retarded manner compared with the wild type. Appressorium of the mck1 mutant was unable to penetrate into plant tissues, thereby rendering the mutant nonpathogenic. Cytorrhysis assay and monitoring of lipid mobilization suggested that the appressorial wall was altered, presumably affecting the level of turgor pressure within appressorium. Furthermore, the mck1 mutant failed to grow inside plant tissue. Complementation of the mutated gene restored its ability to cause disease symptoms, demonstrating that MCK1 is required for fungal pathogenicity. Taken together, our results suggest that MCK1 is an MAPKKK involved in maintaining cell wall integrity of M. oryzae, and that remodeling of the cell wall in response to host environments is essential for fungal pathogenesis.


Author(s):  
Keiko Akagi ◽  
Ming Yi ◽  
Jean Roayaei ◽  
Robert M. Stephens

2011 ◽  
Vol 159 (2) ◽  
pp. 302-315 ◽  
Author(s):  
C. Petri ◽  
J.-M. Hily ◽  
C. Vann ◽  
C. Dardick ◽  
R. Scorza

2015 ◽  
Vol 89 (9) ◽  
pp. 4712-4719 ◽  
Author(s):  
James Justice ◽  
Sanandan Malhotra ◽  
Miguel Ruano ◽  
Yingying Li ◽  
Guillermo Zavala ◽  
...  

ABSTRACTAvian leukosis virus subgroup J (ALV-J) is a simple retrovirus that can cause hemangiomas and myeloid tumors in chickens and is currently a major economic problem in Asia. Here we characterize ALV-J strain PDRC-59831, a newly studied U.S. isolate of ALV-J. Five-day-old chicken embryos were infected with this virus, and the chickens developed myeloid leukosis and hemangiomas within 2 months after hatching. To investigate the mechanism of pathogenesis, we employed high-throughput sequencing to analyze proviral integration sites in these tumors. We found expanded clones with integrations in theMETgene in two of the five hemangiomas studied. This integration locus was not seen in previous work characterizing ALV-J-induced myeloid leukosis.METis a known proto-oncogene that acts through a diverse set of signaling pathways and is involved in many neoplasms. We show that tumors harboringMETintegrations exhibit strong overexpression ofMETmRNA.IMPORTANCEThese data suggest that ALV-J induces oncogenesis by insertional mutagenesis, and integrations in theMEToncogene can drive the overexpression ofMETand contribute to the development of hemangiomas.


NAR Cancer ◽  
2021 ◽  
Vol 3 (2) ◽  
Author(s):  
Adrienne Vancura ◽  
Andrés Lanzós ◽  
Núria Bosch-Guiteras ◽  
Mònica Torres Esteban ◽  
Alejandro H Gutierrez ◽  
...  

Abstract Long non-coding RNAs (lncRNAs) play key roles in cancer and are at the vanguard of precision therapeutic development. These efforts depend on large and high-confidence collections of cancer lncRNAs. Here, we present the Cancer LncRNA Census 2 (CLC2). With 492 cancer lncRNAs, CLC2 is 4-fold greater in size than its predecessor, without compromising on strict criteria of confident functional/genetic roles and inclusion in the GENCODE annotation scheme. This increase was enabled by leveraging high-throughput transposon insertional mutagenesis screening data, yielding 92 novel cancer lncRNAs. CLC2 makes a valuable addition to existing collections: it is amongst the largest, contains numerous unique genes (not found in other databases) and carries functional labels (oncogene/tumour suppressor). Analysis of this dataset reveals that cancer lncRNAs are impacted by germline variants, somatic mutations and changes in expression consistent with inferred disease functions. Furthermore, we show how clinical/genomic features can be used to vet prospective gene sets from high-throughput sources. The combination of size and quality makes CLC2 a foundation for precision medicine, demonstrating cancer lncRNAs’ evolutionary and clinical significance.


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