Use of a non-homologous end-joining-deficient strain (delta-ku70) of the biocontrol fungusTrichoderma virensto investigate the function of the laccase genelcc1in sclerotia degradation
✍ Scribed by Valentina Catalano; Mariarosaria Vergara; Jasmin R. Hauzenberger; Bernhard Seiboth; Sabrina Sarrocco; Giovanni Vannacci; Christian P. Kubicek; Verena Seidl-Seiboth
- Publisher
- Springer-Verlag
- Year
- 2010
- Tongue
- English
- Weight
- 409 KB
- Volume
- 57
- Category
- Article
- ISSN
- 0172-8083
No coin nor oath required. For personal study only.
✦ Synopsis
The aim of this study was to apply a generated Δ__tku70__ strain with increased homologous recombination efficiency from the mycoparasitic fungus Trichoderma virens for studying the involvement of laccases in the degradation of sclerotia of plant pathogenic fungi. Inactivation of the non-homologous end-joining pathway has become a successful tool in filamentous fungi to overcome poor targeting efficiencies for genetic engineering. Here, we applied this principle to the biocontrol fungus T. virens, strain I10, by deleting its tku70 gene. This strain was subsequently used to delete the laccase gene lcc1, which we found to be expressed after interaction of T. virens with sclerotia of the plant pathogenic fungi Botrytis cinerea and Sclerotinia sclerotiorum. Lcc1 was strongly upregulated at early colonization of B. cinerea sclerotia and steadily induced during colonization of S. sclerotiorum sclerotia. The Δ__tku70__Δ__lcc1__ mutant was altered in its ability to degrade the sclerotia of B. cinerea and S. sclerotiorum. Interestingly, while the decaying ability for B. cinerea sclerotia was significantly decreased, that to degrade S. sclerotiorum sclerotia was even enhanced, suggesting the operation of different mechanisms in the mycoparasitism of these two types of sclerotia by the laccase LCC1.