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2021 ◽  
Vol 19 (2) ◽  
pp. 121-129
Author(s):  
Nina V. Mironenko ◽  
Aleksandra S. Orina ◽  
Nadezhda M. Kovalenko

BACKGROUND: The phytotoxin Ptr ToxB as well as Ptr ToxA is one of the pathogenic factors of Pyrenophora tritici-repentis, that cause leaf chlorosis on susceptible wheat varieties, and is encoded by ToxB gene. P. tritici-repentis strains with ToxB gene are rather rare worldwide. MATERIALS AND METHODS: The object of the study was 37 strains isolated from the leaves of wheat grown in Greece. The virulence of the strains was analyzed and the presence of effector genes as well as the average copy number of ToxB was determined. RESULTS: The race composition of P. tritici-repentis population turned out to be mainly represented by the avirulent race 4 (50% of the strains). Strains of race 1 were not found, while strains of other races were found with a low frequency in the population. All analyzed P. tritici-repentis strains had ToxB gene in the genome, while its homologues and ToxA gene were not detected. The average copy number (R) of ToxB in three P. tritici-repentis strains varied from 0.24 to 1.22. The average copy number of ToxB in the mitotic generation of P. tritici-repentis Gr8 strain, which was characterized by the lowest value of R = 0.24, varied from 0.01 to 0.74 and, on average, turned out to be 2 times higher than in the original strain Gr8. CONCLUSION: Presumably, P. tritici-repentis has a mechanism that gives ToxB+ nuclei an advantage in the division rate over ToxB nuclei. This mechanism indicates the existence of an additional function of this gene that is not associated with pathogenicity.


2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Emiliano Pereira-Flores ◽  
Frank Oliver Glöckner ◽  
Antonio Fernandez-Guerra

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2054-2054
Author(s):  
Masao Nakagawa ◽  
Aya Oshiro ◽  
Hiroyuki Tagawa ◽  
Sivasundaram Karnan ◽  
Shinobu Tsuzuki ◽  
...  

Abstract Peripheral T-cell lymphoma, unspecified (PTCL-U) is the most common group among Peripheral T-cell lymphomas (PTCLs). This category consists of the cases which do not belong to any of the recognizable subtypes of PTCLs in WHO classification. PTCL-U comprises heterogeneous groups in morphology and phenotype. Molecular basis of clinical heterogeneity is needed to identify distinct subgroups with clnical relevance. Several reports of conventional cytogenetic studies including comparative genomic hybridization (CGH) showed some recurrent aberrations, but failed to identify the genetic hallmarks to categorize distinct subgroups. So far, no array-based comparative genomic hybridization (array CGH) study for PTCL-U has been reported. Here we analyzed 29 cases of PTCL-U by means of array CGH consisting of 2265 artificial chromosome clones that cover the whole genome at a 1.3 mega base resolution. The analysis clearly divided these cases into two distinct subgroups on the basis of frequency of genomic alterations. One group consists of 17 cases which showed significant lower copy number changes (average copy number gains: 0.5 regions, average copy number losses: 0.1 regions). The other group had average copy number gains of 15.7 regions and losses of 15.0 regions in 12 cases. We designate the former as “simple type” and the latter as “complex type”. In the complex type, regions of recurrent (>20%) gain are detected on chromosome 1q23.3-24.2, 3q25.31-tel, 4p15.1-16.1, 4q28.3-31.23, 5q34, 6p24.1-25.1, 7p21.3-tel, 7p21.1, 7q, 8q24.23, 11q13.4-tel, 12p11.21-11.22, 16p12.3-13.3, 17q11.2-22. Regions of recurrent (>20%) losses are detected on chromosome 1p13.1-13.3, 2q37.3, 4q21.21-21.23, 4q34.3-35.1, 5q21.2-23.1, 6p12.1-q14.3, 6q23.2-24.1, 6q25.1-26, 7p14.3-22.1, 9p21.3, 10p14-qtel, 12p13.1-13.2, 13, 14q12, 16q, 17p, 18p, 20q13-2, 22q11.21-12.2. Median age is 62 years in the simple type and 73 years in the complex type, respectively. Median survival is 27 months in the simple type and 11 months in the complex type. Log-rank test for overall survival between the simple type and the complex type showed inferior survival for the complex type but significance was marginal (p=0.21). Our findings showed that PTCL-U comprised two genetically distinct subgroups, implying that distinct mechanisms underlay in molecular pathogenesis of PTCL-U. Furthermore cilinicopathological features of each group are also being studied.


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