Resistance to Late Blight in Potato - Translational Genomics for Crop Breeding: Biotic Stress - page 228

else they have in common is that their prod-
ucts are involved in recognition of the same
RXLR effector PiAVR2 (Lokossou et al. 2009).
Presence/absence polymorphisms and differen-
tial transcription of this effector explain the viru-
lence of P. infestans isolates on R2 plants (Gilroy
et al. 2011). A method based on the polymor-
phism within the Rpi NBS domain sequences
called NBS-profiling resulted in identification
of a new member of the R2 family, Rpi-snk1 ,
within the species S. schenckii (Jacobs et al.
2010). This finding was further confirmed by
effectoromics, that is, screening Solanum geno-
types with P. infestans effectors for the hypersen-
sitive reactions and R2 allele mining. Apart from
Rpi-snk1 , Rpi-snk1.2 from the same species, Rpi-
edn1.1 from S. edinense and Rpi-hjt1.1-1.3 from
S. hjertingii were localised to the R2 cluster,
cloned, and shown to recognize PexRD11 and
PiAvr2 effectors (Champouret 2010; Verzaux
2010).Within S. brachistotrichum ,an Rpi-bst1
gene was mapped to the Rpi cluster on chromo-
some IV and the cloning of this gene was begun
(Hein et al. 2009).
Several QTLs for late blight resistance span-
ning the same region have been discovered
in different mapping populations (Leonards-
Schippers et al. 1994; Oberhagemann et al.
1999; Collins et al. 1999; Sandbrink et al. 2000;
Sliwka et al. 2007; Danan et al. 2009), and this
resulted in locating there a meta-QTL for this
trait (Danan et al. 2011). QTLs for maturity
were detected in the same region in two stud-
ies (Collins et al. 1999; Bormann et al. 2004).
A QTL for resistance to P. infestans on chro-
mosome IV originated from many wild species
and two of them repeat in independent studies:
S. spegazzinii (Leonards-Schippers et al. 1994;
Danan et al. 2009), and S. microdontum (Sand-
brink et al. 2000; Sliwka et al. 2007). The resis-
tance from S. microdontum , although quantita-
tive and expressed in the field conditions, was
later defined more precisely as encoded by a sin-
gle locus, R Pi-mcd1 (Tan et al. 2008). The R Pi-mcd1
gene was then used in gene pyramiding together
with R Pi-ber . Its effect was rather weak, that is,

it caused a delay of three days to reach 50%
infection. However, there was an additive effect,
suggesting that R Pi-mcd1 can be still useful for
potato breeding programs (Tan et al. 2010). The
last gene of the R2 cluster to be identified so
far is Rpi-dmsf1 , originating most likely from S.
demissum and shown to provide quantitative and
potentially durable resistance that was also tested
in the field (Hein et al. 2007; Hein et al. 2009).

Rpi-blb2

The Rpi-blb2 gene was first mapped in
tetraploid backcross populations derived from
ABPT materials mentioned above (Hermsen
and Ramanna 1973; van der Vossen et al. 2005).
Its position on chromosome VI corresponded
to the position of the tomato Mi-1 gene for
resistance to nematodes, aphids, and white flies.
A more precise map was constructed using F1
progeny of intraspecific S. bulbocastanum cross,
and the Rpi-blb2 gene was positionally cloned
and shown to be a close homolog of the Mi-1
gene, within the CC-NBS-LRR gene family
(van der Vossen et al. 2005). It was detected
in ABPT-derived cultivars Toluca and Bionica
(Vleeshouwers et al. 2011a). Alone or together
with the Rpi-blb1 ,the Rpi-blb2 gene is also being
introduced into potato cultivars via cisgenesis
(Haverkort et al. 2009). One such cisgenic cul-
tivar, Fortuna, with both Rpi-blb1 and Rpi-blb2
genes, is now being tested in advanced field trials
by BASF (Web site: http://www.basf.com/group/
corporate/en_GB/function/conversions:/publish/
content/products-and-industries/biotechnology/
images/Fortuna_VC.pdf). H owever, P. infestans
isolates able to infect plants with each of these
two genes separately or even stacked together
were found in a Dutch population of this
pathogen in the years 2007-2008 (Forch et al.
2010). Avrblb2 effector is an RXLR gene and
belongs to the Avrblb2 family, which is highly
variable and under diversifying selection (Oh
et al. 2009). It accumulates around haustoria
and significantly enhances susceptibility of the
host plant to P. infestans (Bozkurt et al. 2011).