In the years following the rediscovery of Mendel's work, the idea that
a number Mendelian factors are necessary to explain the inheritance of
many QTs became commonplace. Precisely the same experiments supporting
this conclusion in those days are common today. Two inbred lines
(e.g. of mice) with very different QT levels, say H for high, and L
for low, are crossed, resulting in an 
generation which may have
high, low or intermediate phenotypic values. Then an 
intercross
is conducted and we often find that few if any of the resulting progeny
exhibit QT values as high, say, as the H parental line. If the H-L
difference was determined by a single segregating locus, we would
expect 1/4 of the 
progeny to be H; if two independently
segregating loci, 1/16; and so on. Suppose that we had 400 
progeny, and none possessed as high QT values as those in the H
parental line; what could be going on? A natural answer is that there
are likely to be at least 4, 5 or maybe more segregating loci, leading
to 1/256, 1/1024 .. of the 
individuals with the genotype of the
H line. Of course the real story may be much more complicated: there
may be complementary or interacting loci, partial dominance, or one of
many more possibilities such as sex-specific effects, effects
depending on the sex of the parent passing on an allele, and so
on. Even in such a simple thing as an 
intercross between two pure
lines, it is no easy task to determine how many loci must be involved,
and in what way, to explain the differences in a QT.
Let's look at some classic data of East (1916) on corolla length in varieties
of Nicotiana longiflora, a member of the genus that includes
tobacco plants. It illustrates the points I have just made. Two
varieties, 383 and 330 exhibited large differences in corolla length,
and their 
gave plants with intermediate lengths.
The main message of this table is that in neither of the 
generations (well over 400 progeny) do we see phenotypes as extreme as
those in the 383 line.
Although we do not have time to document the assertion fully, we can say that it is now widely believed that the inheritance of QTs can be adequately explained by multiple unlinked or linked Mendelian factors, not in any fundamental way different from those that are invoked to explain qualitative traits. We turn now to modern efforts to map QT loci (QTL).