Agriculture Reference
In-Depth Information
ING LOCUS T
(
FT
), and both genes are an
important part of the photoperiod response
pathway (Kojima and Ogihara 1998). To test
FT
as a candidate for
VRN-B3
, a PCR-based marker
was developed based on the available sequence
information for the barley
FT
orthologue. The
wheat
FT
orthologue cosegregated with
VRN-
B3
. Cosegregation between
FT
and
VRN-H3
was also observed in two low-resolution barley
mapping populations and also in a high-density
mapping population of 800 F
2
plants. Physical
mapping using
FT
and closely linked markers was
conducted in barley and resulted in three contigs
separated by two gaps. One representative BAC
clone for each of the contigs was sequenced. The
genetic map location of two markers developed
from the BAC sequence narrowed the location of
VRN-H3
down to a 0.2-cM interval that con-
tained only the
FT
gene. Spring habit in the
Chinese Spring (Hope 7B) substitution line was
caused by the presence of a long terminal repeat
(LTR) retrotransposon that had inserted into the
FT
promotor. The
FT
transcript levels in winter
plants were low and were upregulated by vernal-
ization. In spring plants,
FT
transcript levels
increased with development. The
FT
gene's
identity as
VRN-3
was confi rmed by transgenic
analysis (Yan et al., 2006).
mapping of these markers. The result was a 263-
kb contig (Faris et al., 2003). The closest distal
marker to
Q
was located at 0.2 cM, but no proxi-
mal markers were identifi ed. Three markers span-
ning approximately 70 kb cosegregated with
Q
.
One of the markers was the orthologue of the
Arabidopsis
fl oral homoeotic gene
APETALA2
(
AP2
).
Since
Q
had been hypothesized to be a major
regulatory gene for fl ower development,
AP2
was
considered a good candidate for
Q
. Comparison
of a Chinese Spring (
Q
) EST for
AP2
present in
Genbank with the sequence of the
T. monococcum
(
q
)
AP2
gene identifi ed at least two amino acid
differences, which could be critical to
AP2
activ-
ity. Twenty-six fast neutron mutants that had lost
the square-headed phenotype were homozygous
or hemizygous for deletions in the
AP2
gene. The
Q
gene is ineffective in the hemizygous condition
and plants with a single functional
AP2
gene have
the speltoid phenotype. The region spanned by
one of the deletions confi rmed that the 260 kb
contig indeed spanned the
Q
region (Faris et al.,
2003). Validation of
AP2
as the gene that under-
lies
Q
was accomplished by isolating the full-
length
AP2
gene from Chinese Spring wheat and
comparing the Chinese Spring sequence with
homologues isolated from Chinese Spring EMS
mutants. All three EMS mutants with speltoid
heads carried single base-pair mutations resulting
in either an amino acid substitution or affecting
intron-exon splice sites. The amino-acid substi-
tution greatly reduced the ability of the
AP2
protein to form a homodimer (Simons et al.,
2006). The identity of
AP2
as
Q
was also con-
fi rmed by transgenic analysis.
Q
The
Q
gene confers the square-headed and free-
threshing phenotype of domesticated wheat and
also affects some other domestication-related
characters. Phenotypic analysis of CS deletion
lines showed that
Q
was located in a submicrosco-
pic region on 5AL defi ned by the terminal dele-
tion lines 5AL-7 and 5AL-23 (Faris and Gill
2002). Differential cDNA and AFLP display on
the 5AL-7 and 5AL-23 lines identifi ed a number
of markers located in that region. Mapping of
these markers in a low-resolution mapping popu-
lation of 190 F
2
plants delineated the
Q
region to
2 cM. The marker most closely linked to
Q
, at
0.7 cM, was used to initiate a chromosome walk,
consisting of multiple cycles of screening the
T.
monococcum
BAC library, sequencing of selected
BAC clones, marker development, and genetic
Ph1
The pairing control gene,
Ph1
, limits pairing of
chromosomes in tetraploid and hexaploid wheats
to homologous chromosomes (Riley and Chapman
1958). It is thought that pairing control originated
in wheat following polyploidization, because
Ph1
activity is absent in the diploid progenitors
(Chapman and Riley 1970). The isolation of
Ph1
was complicated by the fact that no phenotypic
variation existed at this locus. Attempts to induce
