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Proc Natl Acad Sci U S A. 2014 Nov 4;111(44):15711-6. doi: 10.1073/pnas.1411089111. Epub 2014 Oct 20.

Baculovirus resistance in codling moth is virus isolate-dependent and the consequence of a mutation in viral gene pe38.

Author information

1
Institute for Biological Control, Federal Research Center for Cultivated Plants, Julius Kühn-Institut, 64287 Darmstadt, Germany; and.
2
Institute for Biological Control, Federal Research Center for Cultivated Plants, Julius Kühn-Institut, 64287 Darmstadt, Germany; and Department of Phytopathology, Agricultural Service Center Palatinate (DLR Rheinpfalz), 67435 Neustadt an der Weinstrasse, Germany.
3
Department of Phytopathology, Agricultural Service Center Palatinate (DLR Rheinpfalz), 67435 Neustadt an der Weinstrasse, Germany.
4
Institute for Biological Control, Federal Research Center for Cultivated Plants, Julius Kühn-Institut, 64287 Darmstadt, Germany; and Department of Phytopathology, Agricultural Service Center Palatinate (DLR Rheinpfalz), 67435 Neustadt an der Weinstrasse, Germany johannes.jehle@jki.bund.de.

Abstract

The baculovirus Cydia pomonella granulovirus (CpGV) is widely applied as a biocontrol agent of codling moth. After field resistance of codling moth populations had been observed against the commercially used Mexican (M) isolate of CpGV, infection experiments of larvae of the resistant codling moth strain CpRR1 showed that several other naturally occurring CpGV isolates (I12, S, E2, and I07) from different geographic origins are still infectious to resistant CpRR1. Whole-genome sequencing and phylogenetic analyses of these geographic CpGV variants revealed that their genomes share only a single common difference from that of CpGV-M, which is a mutation coding for a repeat of 24 nucleotides within the gene pe38; this mutation results in an additional repeat of eight amino acids that appears to be inserted to PE38 of CpGV-M only. Deletion of pe38 from CpGV-M totally abolished virus infection in codling moth cells and larvae, demonstrating that it is an essential gene. When the CpGV-M deletion mutant was repaired with pe38 from isolate CpGV-S, which originated from the commercial product Virosoft and is infectious for the resistant codling moth strain CpRR1, the repaired CpGV-M mutant was found to be fully infectious for CpRR1. Repair using pe38 from CpGV-M restored infectivity for the virus in sensitive codling moth strains, but not in CpRR1. Therefore, we conclude that CpGV resistance of codling moth is directed to CpGV-M but not to other virus isolates. The viral gene pe38 is not only essential for the infectivity of CpGV but it is also the key factor in overcoming CpGV resistance in codling moth.

KEYWORDS:

Cydia pomonella granulovirus; codling moth; genome sequencing; mutation; resistance; resistance management

PMID:
25331863
PMCID:
PMC4226074
DOI:
10.1073/pnas.1411089111
[Indexed for MEDLINE]
Free PMC Article

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