Resistance gene analogues as a tool for basic and applied resistance genetics exemplified by sugarcane mosaic virus resistance in maize (Zea mays L.) [Elektronische Ressource] / Marcel Quint

Quint

Informations

• Publié par: universitat_hohenheim
• Publié le: 01 janvier 2004
• Nombre de lectures: 5
• Langue: English
• Poids de l'ouvrage: 2 Mo

Extrait

Die vorliegende Arbeit wurde am 21.01.2003 von der Fakultät III – Agrarwissenschaften der
Universität Hohenheim als Dissertation zur Erlangung des Grades eines Doktors der
Agrarwissenschaften (Dr. Sc. Agr.) angenommen.

Tag der mündlichen Prüfung: 31.01.2003
Prodekan: Prof. Dr. K. Stahr
Berichterstatter, 1. Prüfer: Prof. Dr. A.E. Melchinger
Mitberichterstatter, 2. Prüfer: Prof. Dr. A. Pfitzner
Mitberichterstatter, 3. Prüfer: Prof. Dr. R. Blaich Aus dem Institut für
Pflanzenzüchtung, Saatgutforschung und Populationsgenetik
der Universität Hohenheim
Fachgebiet Angewandte Genetik und Pflanzenzüchtung
Prof. Dr. A.E. Melchinger



Resistance gene analogues as a tool for basic
and applied resistance genetics exemplified
by sugarcane mosaic virus resistance in
maize (Zea mays L.)



Dissertation
zur Erlangung des Grades eines
Doktors der Agrarwissenschaften
der Fakultät III – Agrarwissenschaften
der Universität Hohenheim


von Dipl.-Ing. sc. agr.
Marcel Quint
aus
Celle


Stuttgart-Hohenheim
2002 Contents


1 General introduction 1

12 Breeding for virus resistance in maize 11

3 Development of RGA-CAPS markers and genetic mapping of candidate 28
2genes for sugarcane mosaic virus resistance in maize

4 Conversion of fragments tightly linked to SCMV resistance genes Scmv1 37
3and Scmv2 into simple PCR-based markers

5 Identification of genetically linked RGAs by BAC screening in maize and 43
4implications for gene cloning, mapping, and MAS

56 Duplicate marker loci can result in incorrect locus orders on linkage maps 50

7 General discussion 62

8 Summary 74

9 Zusammenfassung 77
10 Acknowledgements 80
11 Curriculum vitae 81




1Quint M, Melchinger AE, Dußle CM, Lübberstedt T (2000) Breeding for virus
resistance in maize. Genetika 32:529-545
2Quint M, Mihaljevic R, Dußle CM, Xu ML, Melchinger AE, Lübberstedt T (2002)
Development of RGA-CAPS markers and genetic mapping of candidate
genes for sugarcane mosaic virus resistance in maize. Theor. Appl. Genet.
105: 355-363
3Dußle CM, Quint M, Xu ML, Melchinger AE, Lübberstedt T (2002) Conversion of
fragments tightly linked to SCMV resistance genes Scmv1 and Scmv2 into
simple PCR-based markers. Theor. Appl. Genet. 105: 1190-1195
4Quint M, Dußle CM, Melchinger AE, Lübberstedt T (2003) Identification of
genetically linked RGAs by BAC screening in maize and implications for
gene cloning, mapping, and MAS. Theor. Appl. Genet. 106: 1171-1177
5Frisch M, Quint M, Lübberstedt T, Melchinger AE (2004) Duplicate marker loci can
result in incorrect locus orders on linkage maps. Theor. Appl. Genet. (in
press)
iAbbreviations
Abbreviations

AFLP amplified fragment length polymorphism
Avr gene avirulence gene
ATP adenosine triphosphate
BAC bacterial artificial chromosome
BSA bulked segregant analysis
CAPS cleaved amplified polymorphic sequence
DNA deoxyribonucleic acid
GTP guanosine triphosphate
EST expressed sequence tag
indel insertion/deletion
JGMV Johnson grass mosaic virus
LRR leucine-rich repeat
MAS marker-assisted selection
MDMV maize dwarf mosaic virus
MHC major histocompatibility complex
NBS nucleotide bindinge site
ORF open reading frame
PCR polymerase chain reaction
QTL quantitative trait locus/loci
RGA resistance gene analogue
R gene resistance gene
SCMV sugarcane mosaic virus
SSR simple sequence repeat
SNP single nucleotide polymorphism
SrMV Sorghum mosaic virus
STS sequence tagged site
TIR Toll and interleukin receptor-like
WSMV wheat streak mosaic virus




iiGeneral introduction
1 General introduction


Plant disease resistance

Plants are continually exposed to pathogen attack, but diseases are rare. There are
basically three reasons for the missing success of pathogen infection and reproduction. (1)
The plant does not supply the essential living requirements for a potential pathogen and is
therefore a non-host. (2) Preformed plant defense compounds like structural barriers or
pathotoxins restrict successful pathogen infection. (3) Plants are capable of defending
themselves by means of a combination of constitutive and induced defenses. The latter
resistance mechanism depends on recognition of the attacking pathogen. Knowledge about the
genetic and biochemical basis of plant disease resistance has accumulated since the turn of the
previous century, when plant breeders first recognised that disease was often controlled by
Mendelian genes (Biffen 1905). The plant kingdom contains thousands of resistance genes (R
genes) with specificities for particular viral, bacterial, fungal, or nematode pathogens. Despite
the differences in defense responses induced by different plant-microbe interactions, some
common characteristics are apparent during R gene mediated defenses. Therefore, it is
becoming evident that plant genomes contain a large number of genes that are involved in the
detection and discrimination of potential pathogens. Usually, the function of a certain R gene
is limited to one or few genotypes of the respective pathogen (Keen 1992, de Wit 1992).
Generally, plant disease resistances can be inherited in a monogenic, oligogenic, or
polygenic manner. Therefore, qualitative and quantitative resistances have to be distinguished
concerning their resistance mechanism.


Qualitative resistance

The resistance mechanism of plants conferring qualitative or monogenic inherited
resistance is comparable to the mammalian immune system with production of antigens by
mammalian pathogens. Plant pathogens also produce a variety of potential signals. Some of
these signals are detectable by plants. Genes expressing these signals in the pathogen are
1General introduction
designated avirulence (Avr) genes. Equivalent matching R and Avr gene pairs enable
recognition of the pathogen and induce defense responses. Therefore, R gene products can be
described as receptors for Avr-coded ligands in a gene-for-gene relationship (Flor 1956,
1971). R-Avr gene pairs resulting in resistance are epistatic over gene pairs that would
otherwise result in susceptibility (Crute and Pink 1996). Gene pairs conferring higher degrees
of resistance are generally epistatic over gene pairs associated with lower degrees of
resistance, although phenotypic variation indicative of genetic additivity has also been
reported, when more than one gene pair conferring resistance is effective. Following pathogen
recognition, the resistance protein is presumed to activate signalling cascades that coordinate
the initial plant defense response to impair pathogen ingress. Early signalling events
following recognition are for example activation of protein kinases, induction of ion fluxes
across the cellular membrane, and the release of reactive oxygen species probably triggering
the transcriptional activation of defense responses. This signalling cascade results in the
production of salicylic acid, cell wall fortification, and the expression of pathogenesis related
proteins (reviewed in Hammond-Kosack and Jones 1996). Therefore, disease resistance
triggered by genotype-specific pathogen recognition also became a model for signal
transduction in plants.


Quantitative resistance

Polygenic or oligogenic inherited resistances are generally thought to be more durable
and stable than monogenic resistances due to race or isolate unspecificity. The resulting
resistance is caused by mechanisms different from the classical gene-for-gene concept and the
subsequent hypersensitive response. The diversity of traits by which quantitative resistance
can be expressed can be attributed to the variability of resistance mechanisms targeted at the
mode of infection and the postinfectious effects of the virus. The defense response may be
expressed in reduced rates of infection. Postinfectious mechanisms may cause extended
incubation times, reduced virus concentration, incomplete virus spread, or reduction of the
virus caused growth and yield losses.
The peculiarity of the re