448
T . C . HSU
an ovum with X 2 , when being fertilized by a Y-bearing sperm, changes
to X 2 ; and when X 2 and X 2 are together in a female zygote, one of them
is converted (by George!) to X 2 . This is likewise unsatisfactory. Yet the
fact remains that the two X chromosomes of the Chinese hamster are
more or less different in morphology as well as in D N A synthetic cycle.
Referring to the hypothesis of gene inactivation in relation to chromosome condensation, it does not appear difficult to propose a generalization. Let us assume that the two X chromosomes of any female cell
are identical in their genetic background and either of them can fertilize with any sperm to produce viable progeny. This agrees with the
classical X X - X Y sex determination mechanism. Let us first consider
the case of man and the majority of mammals. Sometime during the
process of female embryonic development, one of the X elements in the
somatic tissues becomes inactivated by the allocycly or out-of-phase
condensation system. From this stage onward, the nuclei will bear the
sex chromatin and the X chromosome will show heteropyknosis in
prophase. Once the chromosome is inactivated, it is not reversible as
far as the somatic cell lineage is concerned.
If the foregoing discussion does not seem unreasonable, it would then
be relatively simple to apply a modified hypothesis to fit the situation
existing in Chinese hamster cells. First, as Matthey (1961) pointed out,
the sex chromosomes of many species of paleoarctic Cricetinae have
a section of autosome translocated on to them. This may account for
the somewhat unusual sex chromosome pair of the Chinese hamster,
which, however, is immaterial in our interpretation of the sex determination system. Here the only modification from the conventional
type just postulated is that, during female embryonic development,
different sections of the two X chromosomes become inactivated in
somatic tissues. The two X chromosomes appear morphologically
different because of different allocycly systems, but they are genetically
identical. Personally, I think the difficulty in explaining the nature
of the sex chromosomes in mammalian species rests upon the concept
of rigid localization of heterochromatin, the concept that whenever
a chromosome or a part of a chromosome shows heteropyknosis, it is
genetically different from the euchromatin. It seems more plausible to
regard the phenomenon of heteropyknosis or allocycly as a physiological
response of the chromosome to the environment instead of intrinsic
difference.
The inactivation concept elicits several new questions. (1) Which
X chromosome in the female cells becomes inactivated, the paternal
or the maternal? (2) When does this inactivation take place? (3) Since
one of the X's is inactivated in the somatic tissues, does it mean that
normal females are equivalent to an X O female?
T . C . HSU
an ovum with X 2 , when being fertilized by a Y-bearing sperm, changes
to X 2 ; and when X 2 and X 2 are together in a female zygote, one of them
is converted (by George!) to X 2 . This is likewise unsatisfactory. Yet the
fact remains that the two X chromosomes of the Chinese hamster are
more or less different in morphology as well as in D N A synthetic cycle.
Referring to the hypothesis of gene inactivation in relation to chromosome condensation, it does not appear difficult to propose a generalization. Let us assume that the two X chromosomes of any female cell
are identical in their genetic background and either of them can fertilize with any sperm to produce viable progeny. This agrees with the
classical X X - X Y sex determination mechanism. Let us first consider
the case of man and the majority of mammals. Sometime during the
process of female embryonic development, one of the X elements in the
somatic tissues becomes inactivated by the allocycly or out-of-phase
condensation system. From this stage onward, the nuclei will bear the
sex chromatin and the X chromosome will show heteropyknosis in
prophase. Once the chromosome is inactivated, it is not reversible as
far as the somatic cell lineage is concerned.
If the foregoing discussion does not seem unreasonable, it would then
be relatively simple to apply a modified hypothesis to fit the situation
existing in Chinese hamster cells. First, as Matthey (1961) pointed out,
the sex chromosomes of many species of paleoarctic Cricetinae have
a section of autosome translocated on to them. This may account for
the somewhat unusual sex chromosome pair of the Chinese hamster,
which, however, is immaterial in our interpretation of the sex determination system. Here the only modification from the conventional
type just postulated is that, during female embryonic development,
different sections of the two X chromosomes become inactivated in
somatic tissues. The two X chromosomes appear morphologically
different because of different allocycly systems, but they are genetically
identical. Personally, I think the difficulty in explaining the nature
of the sex chromosomes in mammalian species rests upon the concept
of rigid localization of heterochromatin, the concept that whenever
a chromosome or a part of a chromosome shows heteropyknosis, it is
genetically different from the euchromatin. It seems more plausible to
regard the phenomenon of heteropyknosis or allocycly as a physiological
response of the chromosome to the environment instead of intrinsic
difference.
The inactivation concept elicits several new questions. (1) Which
X chromosome in the female cells becomes inactivated, the paternal
or the maternal? (2) When does this inactivation take place? (3) Since
one of the X's is inactivated in the somatic tissues, does it mean that
normal females are equivalent to an X O female?