Some possible bearings of genetics on pathologyMorgan, Thomas Hunt
Science
Some possible bearings of genetics on pathology
Morgan, Thomas Hunt
Diseases -- Causes and theories of causation; Genetics; Heredity; Pathology
Before we take up the main questions before us this evening, I must speak
of one other form of heredity. In many instances we have evidence that
a character is the product of more than a single _mutant_ gene. I say
“mutant gene” because in fact every character is no doubt the product
of the combined action of many genes, but in addition to this general
relation there are many cases now known where there are several specific
genes whose _chief_ effect is on one character. Size differences furnish
abundant data of this sort. One of the clearest cases is that of the size
of the ear of corn. Some races of corn have short ears (and cobs), some
long. If two such races are crossed, the hybrid is intermediate with a
considerable range of variation. If the hybrid is self-fertilized, the
progeny in the next generation shows a still wider range of variation,
extending from that of the shorter grandparent to that of the longer.
Both grandparental cobs have reappeared, but also many intermediate
grades, Fig. 5.
[Illustration: FIG. 5. Cross between long- and short-eared corn. Samples
of two original types shown in upper part of figure, hybrid offspring in
the middle of figure, and samples of 2d generation in the lower part.
(After East and Hays.)]
Such cases were formerly spoken of as blended inheritance. It was
supposed that the materials of the two parents have, as it were, fused
in the offspring and have remained fused. Today we have a better
explanation. It is this. Besides two major factors that here determine
cob length, there are other _minor_ factors, some of which make the
short cob longer, others that make the long cob shorter. These go over
into the first generation hybrids, and are sorted out in the germ cells
of the hybrid. Consequently, when the F₁’s are inbred, there are all
sorts of recombinations of the minor factors. This explains the greater
variability of the second generation.
It is probable that in most of our domesticated animals, including man,
much of the variability is due to multiple factors, which makes a study
of inheritance in these groups extremely difficult, especially when, as
in the case of man, the number of offspring from a pair is small, and
critical combinations for study can not be made.
If then it is highly improbable that any particular defective trait could
ever become widely spread in the human germ-plasm, how does it come about
that such defects as feeblemindedness and insanity are so widespread in
the racial inheritance? There are several possibilities here to keep in
mind, but I think we ought not to pretend that we can give a completely
satisfactory account of the situation.
Public-domain text, read in full here on John Shaqi.
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