450
T . G. HSU
some, the chromatin mass in interphase certainly does not match that
of the chromosomes in metaphase. However, in a case of a presumed
isochromosome of the long arm ofthe X , Jacobs et al. (1961) found onethird of the buccal mucosa cells showing unusually large sex chromatin
and frequently very large drumsticks in leukocytes implying that sex
chromatin may indeed represent the entire X . Nevertheless, more
evidence is required to establish this debatable correlation. Genetic experiments with good markers scattered throughout the X
chromosome would certainly help to clear this point. The hypothesis
could be more flexible if we assume that: (1) the X chromosome needs
not be inactivated along its entire length; and (2) inactivation is not
a complete process.
According to Austin and Amoroso (1957) and Park (1957), sex
chromatin can be detected relatively early in the embryos, generally in
the late blastocyst. It is still an enigma why one of the two X chromosomes should be inactivated in somatic cells of mammals. It is more
conceivable that the X Y pair in male spermatogenesis condense
precociously to prevent possible crossover of genetic materials between
the two elements, especially if they carry sex-determining factors.
However, it becomes unexplainable again why in the grasshopper,
where an X O condition exists, the X chromosome is strongly allocyclic
in the germ line. Probably we will have to be content with whatever
advances have been made, leaving unsolved questions to a later date
when new ideas and new information come along from various research
fields.
If the inactivation hypothesis is correct, does it then mean that a
normal female has actually an X O constitution? In the mouse the
answer appears to be affirmative, because an X O female is normal and
fertile. In man it apparently is not. Patients with Turner's syndrome
are sterile and sexually underdeveloped, and patients with more than
one X and a Y are not bona fide males. Therefore, the supposedly
inactivated X chromosome must contribute something to the over-all
physiology of the bearer. That sex chromatin does not appear during
very early embryonic stages must mean something important to the
development of the zygote; but it is doubtful that the inactivated X
really becomes superfluous after this stage.
No one will deny that the Y chromosome in mammals is strongly
male-determining. Whenever a Y chromosome is present in an individual, the individual is more or less a male, irrespective of the number
of the X chromosomes. It is of interest in this connexion to point out
that the Y chromosome may also be allocyclic (Fig. 11a), which would
suggest that the Y is also inactivated. Then how does the Y chromosome
determine maleness? The situation is probably similar to the inactivated
T . G. HSU
some, the chromatin mass in interphase certainly does not match that
of the chromosomes in metaphase. However, in a case of a presumed
isochromosome of the long arm ofthe X , Jacobs et al. (1961) found onethird of the buccal mucosa cells showing unusually large sex chromatin
and frequently very large drumsticks in leukocytes implying that sex
chromatin may indeed represent the entire X . Nevertheless, more
evidence is required to establish this debatable correlation. Genetic experiments with good markers scattered throughout the X
chromosome would certainly help to clear this point. The hypothesis
could be more flexible if we assume that: (1) the X chromosome needs
not be inactivated along its entire length; and (2) inactivation is not
a complete process.
According to Austin and Amoroso (1957) and Park (1957), sex
chromatin can be detected relatively early in the embryos, generally in
the late blastocyst. It is still an enigma why one of the two X chromosomes should be inactivated in somatic cells of mammals. It is more
conceivable that the X Y pair in male spermatogenesis condense
precociously to prevent possible crossover of genetic materials between
the two elements, especially if they carry sex-determining factors.
However, it becomes unexplainable again why in the grasshopper,
where an X O condition exists, the X chromosome is strongly allocyclic
in the germ line. Probably we will have to be content with whatever
advances have been made, leaving unsolved questions to a later date
when new ideas and new information come along from various research
fields.
If the inactivation hypothesis is correct, does it then mean that a
normal female has actually an X O constitution? In the mouse the
answer appears to be affirmative, because an X O female is normal and
fertile. In man it apparently is not. Patients with Turner's syndrome
are sterile and sexually underdeveloped, and patients with more than
one X and a Y are not bona fide males. Therefore, the supposedly
inactivated X chromosome must contribute something to the over-all
physiology of the bearer. That sex chromatin does not appear during
very early embryonic stages must mean something important to the
development of the zygote; but it is doubtful that the inactivated X
really becomes superfluous after this stage.
No one will deny that the Y chromosome in mammals is strongly
male-determining. Whenever a Y chromosome is present in an individual, the individual is more or less a male, irrespective of the number
of the X chromosomes. It is of interest in this connexion to point out
that the Y chromosome may also be allocyclic (Fig. 11a), which would
suggest that the Y is also inactivated. Then how does the Y chromosome
determine maleness? The situation is probably similar to the inactivated