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Molecular Pathogens
MP 2010, Vol.1, No.1
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Research Article Open Access
Cloning and Analysis of Fusarium Wilt Resistance Gene Analogs in ‘Goldfinger’
Banana
Dequan Sun , Yulin Hu , Lubin Zhang , Yiwei Mo , Jianghui Xie
South Subtropical Crop Research Institute of Chinese Academy of Tropical Agricultural Science, Zhanjiang, 524091
Corresponding author email: xiejianghui@21cn.com;
Authors
Molecular Pathogens 2010, Vol 1 No 1 DOI: 10.5376/mp.2010.01.0001
Received: Sep. 29, 2010
Accepted: Oct. 26, 2010
Published: Oct. 30, 2010
This article was first published in the Molecular Plant Breeding (Regular Print Version), and here was authorized to redistribute under the
terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided
the original work is properly cited.
Preferred citation for this article as:
Sun et al 2009, Cloning and Analysis of Fusarium Wilt Resistance Gene Analogs in ‘Goldfinger’ Banana, Molecular Plant Breeding, 7(6): 1215-1222
Abstract
Based on the conservative regions of the nucleotide-binding site and the leucine-rich repeat (NBS-LRR) in cloned wilt
resistance genes, the polymerase chain reaction with degenerate primers was employed to isolate resistance gene analogues (RGAs)
from the genomic DNA of wilt resistance germplasm ‘Goldfinger’ (AAAB) banana. As a result, twenty fragments of RGAs were
isolated, which were of expected size (about 530 bp). Analysis of the deduced amino acids of these RGAs show that they share the
NB-ARC domain and belong to the non-TIR-NBS class resistance gene candidates, containing 4 conservative amino acid domains,
i.e. P-loop (GMGGVGKTT), Kinase-2 (LLVLDDIW), RNBS-B (CKVLFTTRS), and hydrophobic amino acids GLPL
(GLPLALKVL). Other results reveal that sequence identity among the 20 RGAs rang from 41.1% to 99.3%, while identity of the
deduced amino acid sequences range from 33.2% to 96.3%. The phylogenetic analysis of the RGA nucleotide sequences and the
deduced amino acids showed that the 20 sequences could be divided into 5 distinct types. All of the amino acids deduced from the
RGAs share a homology of 28%~54% with those deduced from the known wilt resistance genes such as Fom-2
，
I2C-1
，
I2C-2 and I2.
This result to some degree indicates the conservation of disease resistance gene evolution. Technically, these RGAs isolated in the
present study would lay a base for the further cloning of wilt resistance genes in banana, which could also be used as molecular
markers for screening candidate wilt resistance genes in banana.
Keywords
Banana, Fusarium wilt, Resistance gene analogs, Nucleotide binding site
Background
Banana (Musa spp.) is one of the most important fruit
crops in the world in terms of production and
consumption. Fusarium wilt is regarded as one of the
most devastating diseases of banana, affecting
plantations in almost all banana-growing countries of
the world (Ploetz et al., 1990). This disease is caused
by the soil-borne fungus Fusarium oxysporum formae
specialis (f. sp.) cubense (FOC) (Stover, 1962). The
fungus, surviving as chlamydospores, will germinate
to infect the lateral or feeder roots when they come
into contact with banana roots (Beckman, 1990). After
infection, the pathogen will colonize and block the
plant's vascular system, a process that leads to wilting,
and eventually, plant mortality (Ploetz and Pegg,
2000). In recent years, Race 4 of this fungous
pathogen (Foc4) has become the most virulent race of
this disease. It can infect almost all the banana and
plantain cultivars, including those that were resistant
to other races of the disease (Ploetz, 1993).
The most common cultivar in worldwide commercial
production is the Cavendish cultivar, which has
resistance to some isolates of FOC (Pegg et al., 1996).
Commercially grown banana plants, which are
clonally propagated, sterile triploid plants, are highly
susceptible to Fusarium wilt due to many factors
(Pegg et al., 1996; Vuylsteke, 2000). Although plant
micropropagation leads to the reduction in the spread
of FOC, it also results in enhanced susceptibility to
FOC for two years after plantlets are removed from
tissue culture (Smith et al., 1998). Options for the
control of Fusarium wilt are limited by ineffectual
chemical control and the lack of commercially
suitable resistant cultivars (Smith et al., 2006). And no
known fungicide is effective in controlling FOC4 up
to now. Hence, the development of new banana