Agriculture Reference
In-Depth Information
Compared with many crop species only a small number of 'qualitative' genes
with easily visible effects have been described in onion. One example is a recessive
gene which, when homozygous, results in dwarf seedstalks. In the heterozygous
condition the seedstalks are of normal length because the allele for normal length
is dominant over that for dwarf. Genetic analyses of onions are time-consuming
because of the biennial generation time and the severe inbreeding depression,
which means that it is difficult to produce and maintain a large number of near-
homozygous inbred lines ideal for genetic linkage analysis. King
et al.
(1998)
stated that just 17 morphological or disease-resistance gene loci had been
described for onion, including those for: colours of bulbs, foliage, anthers and
seedcoats; male fertility restoration in cytoplasmic male-sterility; pink-root resis-
tance; ozone damage resistance; dwarf seedstalk; and four loci deleterious for
chlorophyll.
The colour of onion skins is determined by the combined effect of a number
of major genes, each of which has different alleles causing well-defined
qualitative effects (El-Shafie and Davis, 1967). This is a good example of
'epistasis', an important genetic phenomenon where the interaction of several
different genes determines the outcome, in this case of whether the onion bulb
has a white, yellow or red skin. Many of these epistatic effects have now been
explained in molecular terms. They provide elegant examples of how changes
in chromosomal DNA sequences result in modifications of gene control,
enzyme synthesis or enzyme function to modify a biosynthetic pathway and
thereby the resulting plant (the 'phenotype'). Five major genes affecting bulb
colour were discovered by classic genetic inheritance studies. The interactions
between these genes imply that they act sequentially along the biosynthetic
pathway for anthocyanin pigments (see Fig 3.3; Kim
et al.
, 2004b, 2005a;
Chapter 8, this volume).
First, this pathway depends on the basic colour factor or C gene, which has
both dominant and recessive alleles. White-skinned onions lack the enzyme
chalcone synthase (CHS), so that they do not produce any pigments of the
anthocyanin pathway (see Fig 3.3). The C gene appears to be a regulatory gene
that controls whether or not the genes coding for two CHS enzymes actually
transcribe and initiate the process to synthesize the enzyme proteins (Kim
et al.
,
2005b). Yellow onions from the USA have a deletion in the DNA of the gene that
that transcribes for the enzyme dihydroflavonol 4-reductase (DFR) (see Fig 3.3;
Kim
et al.
, 2004a). This mutation prevents the production of DFR and therefore
blocks the pathway after dihydroquercetin, resulting in the accumulation of the
yellow quercetin pigment without any red cyanidin.
Brazilian yellow onions do produce DFR and also the anthocyanidin
synthase (ANS) protein (see Fig 3.3), but a point nucleotide mutation in the DNA
sequence coding for ANS results in the substitution of the amino acid glycine by
arginine at the corresponding point in the amino acid sequence of the enzyme.
