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

被引：320
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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