Transgenic Applications in Wheat Improvement - Wheat Science and Trade - page 397

were also evident in four years of fi eld trials at
three locations, but only when conditions were
not limiting, that is, in well-spaced plantings (8-9
plants per 3 m row) under irrigation. Transgenic
and non-transgenic plants had the same yields in
rainfed plots planted at standard densities (Meyer
et al., 2007).
Preharvest sprouting compromises wheat end-
use quality. Wilkinson et al. (2005) were able to
reduce the extent of preharvest sprouting by
transforming wheat with an oat VP1 gene under
control of the Ubi1 promoter. The oat gene tran-
script was more effi ciently spliced to coding
mRNA than the endogenous wheat VP1 tran-
scripts, resulting in higher levels of the VP1
protein, which is both a positive regulator of mat-
uration and a negative regulator of germination.
Wheat transformants containing the oat VP1 gene
showed 35% reductions in the number of seeds
that germinated 9 and 14 weeks after anthesis
under cool moist conditions (Wilkinson et al.,
2005).

et al., 2003) and rice (Chen et al., 1999); and (vi)
α-purothionin from wheat (Mackintosh et al.,
2007). To achieve widespread expression through-
out the plant, all coding sequences were controlled
by the maize Ubi1 promoter, except for the maize
b32 gene, which was controlled by the 35 S
promoter.
Makandar et al. (2006) used a strategy designed
to invoke a plantwide defense system to combat
Fusarium head blight. They transformed wheat
with the Arabidopsis NPR1 gene under control
of the maize Ubi1 promoter. This gene encodes
an inducer of systemic acquired resistance. By
expressing this regulator throughout develop-
ment, the investigators hoped to arm the plant
with multiple defense compounds before it was
challenged by the pathogen.
Greenhouse tests of transgenic plants carrying
each of these constructs showed that Type II
resistance improved 20 to 50% compared with
their nontransformed parents. However, when
several of these transgenic plants were challenged
with Fusarium infection in fi eld experiments
(Okubara et al., 2002; Anand et al., 2003;
Mackintosh et al., 2007), only those expressing
the wheat α-thionin, barley β-1,3-glucanase, and
barley tlp showed any improvement in resistance
(Mackintosh et al., 2007). Among these, only a
line carrying the glucanase transgene showed
reduction of multiple disease indices in the fi eld,
including deoxynivalenol accumulation, the per-
centage of visually scabby kernels, and disease
severity, compared with the nontransformed
parent (Mackintosh et al., 2007).
The potential for control of some other fungal
pathogens has been tested by genetic transforma-
tion with genes encoding plant defense proteins
or compounds with known antifungal activity.
Resveratrol is a member of the stilbene family of
phytoalexins. It serves as an antifungal defense
protein in grape ( Vitis vinifera L.) and is also
believed to have positive effects on human health.
Fettig and Hess (1999) transformed wheat plants
with the grapevine stilbene sythase gene under
control of the maize Ubi1 promoter. Four of seven
plants expressed the transgene and were shown to
accumulate resveratrol. Serazetdinova et al. (2005)
transformed wheat with a resveratrol synthase

Applications to improve pathogen and
pest resistance
Another major target for wheat genetic transfor-
mation has been increased resistance to various
plant pathogens and pests. Several strategies
(Dahleen et al., 2001) have been aimed at improv-
ing resistance to Fusarium head blight caused
by Fusarium graminearum Schwabe, a disease of
wheat that decreases yield and contaminates the
grain with mycotoxins. Several genes have shown
promise for limiting the spread of Fusarium within
the spike in greenhouse trials (Type II resistance):
(i) one encoding deoxynivalenol acetyltransferase,
targeted to reduce toxicity of the mycotoxin that
facilitates spread of the fungus (Okubara et al.,
2002); (ii) several encoding cereal-defense pro-
teins, including thaumatin-like proteins (tlps)
from barley (Mackintosh et al., 2007) and rice
(Chen et al., 1999); (iii) class II β-1,3-glucanases
from barley (Mackintosh et al., 2007) and resis-
tant wheat cultivar Sumai 3 (Anand et al., 2003);
(iv) Ribosomal Inhibitory Protein (RIP) b32 from
maize (Balconi et al., 2007); (v) acidic chitinases
from resistant wheat cultivar Sumai 3 (Anand