Agriculture Reference
In-Depth Information
cell (see review by Chisholm
et al.,
2006). Plants have subsequently evolved to produce
proteins that recognise pathogen effector proteins. These resistance or R genes interact
with the pathogen effector genes to produce the classic gene-for-gene resistance response
(Flor, 1971). Pathogen virulence occurs where the pathogen effector protein is modifi ed
in some way such that the resistance gene is no longer as effective in recognising the
effector gene.
Improved host resistance to a wide range of pathogens could be developed by trans-
genic insertion of novel MAMP receptors derived from other species or modifi ed in
some way to broaden their effectiveness. It must be borne in mind however that MAMP-
activated defences may be switched off by pathogens. Problems may also arise if there is
a physiological cost of a plant producing such receptors in the absence of pathogen attack.
Natural resistance genes appear to only trigger host defences when required, minimising
the cost to the host plant. A similar level of fi ne control may be needed for transgenic
resistance and identifying the appropriate promoters and control mechanisms may not be
straightforward.
An option other than inserting novel resistance genes is to modify the expression
of existing ones that are involved in the resistance pathway (reviewed by Rommens &
Kishore, 2000). A successful demonstration of this possibility involved the
NPR
1 gene
in
Arabidopsis
that regulates systemic acquired resistance, overexpression of which
increased the plant's resistance to a diverse array of pathogens (Cao
et al.
, 1998; see also
Chapter 4).
A specifi c option for developing improved resistances to pathogenic viruses has been
to transform the gene that expresses their coat proteins into the host. The effectiveness of
this approach was fi rst demonstrated with tobacco mosaic virus (TMV), where the coat
protein delayed symptoms when inserted into the genome of tobacco plants (Powell-Abel
et al.,
1986).
Papaya ringspot virus (PRSV) is a damaging disease that limits papaya production
worldwide. Soon after the TMV demonstration, a PSRV-resistant line was developed on
Hawaii using transformed PRSV coat protein incorporated into the host genome (Fitch
et al.,
1992). Two varieties, Rainbow and SunUp, were subsequently commercialised
in 1998 and Rainbow, an F1 hybrid developed from a cross between the homozygous
transgenic SunUp and the non-GM variety Kapoho, became widely planted and helped
to save the papaya industry on the island from devastation by PRSV (Gonsalves, 2004).
Transgenic papaya germplasm was also released for commercial cultivation in China in
2006 and is being developed for other papaya growing areas including South-East Asia,
Australia, Brazil and Jamaica. To date, this is the only example of commercial production
of a transgenic crop developed for disease resistance. However, with an increasing number
of genes associated with the host defence response being identifi ed and with increasing
public acceptance of GM technologies, it is expected that varieties with improved disease
resistance will be developed using genetic engineering in the coming years.
6.3.4
Mutation
Mutation provides an attractive option for developing alternative disease resistances where
insuffi cient variation for resistance exists in a crop or a related species. The mutation can be
generated through point mutation by a chemical, typically ethyl methyl sulphonate (EMS)
