The akuBKU80 mutant deficient for nonhomologous end joining is a powerful tool for analyzing pathogenicity in Aspergillus fumigatus

被引：326

作者：

Ferreira, MED

Kress, MRVZ

Savoldi, M

Goldman, MHS

Härtl, A

Heinekamp, T

Brakhage, AA

Goldman, GH

机构：

[1] Univ Sao Paulo, Dept Ciencias Farmaceut, Fac Ciencias Farmaceut, BR-14040903 Ribeirao Preto, SP, Brazil

[2] Univ Sao Paulo, Fac Filosofia Ciencias & Letras Ribeirao Pret, Ribeirao Preto, SP, Brazil

[3] Hans Knoell Inst, Drug Testing Grp, Jena, Germany

[4] Hans Knoell Inst, Dept Mol & Appl Microbiol, Jena, Germany

[5] Hans Knoell Inst, Leibniz Inst Nat Prod Res & Infect Biol, Jena, Germany

来源：

EUKARYOTIC CELL | 2006年 / 5卷 / 01期

关键词：

D O I：

10.1128/EC.5.1.207-211.2006

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

To increase the frequency of homologous recombination, we inactivated the KU80 homologue in Aspergillus fumigatus (named akuB(KU80)). Homologous integration reached about 80% for both calcineurin A (calA) and polyketide synthase pksP (alb1) genes in the akuB KU80 mutant to 3 and 5%, respectively, when using a wild-type A. fumigatus strain. Deletion of akuB KU80 had no influence on pathogenicity in a low-dose murine infection model.

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页码：207 / 211

页数：5

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