12. G E N E T I C C Y T O L O G Y
439
were not; or both could be labeled; or the autosomes could be labeled
while the X remained unlabeled. This situation was similar to that of
the mitotic cells of the Chinese hamster just described. From all
reported cases it seems that chromosomes or chromosome parts, showing
heteropyknosis, synthesize D N A at the time when euchromatin has
completed its D N A replication. It is possible that the asynchronous
DNA synthesis is a direct consequence of the out-of-cycle coiling of
the chromosomes or chromosome parts which are heteropyknotic.
There is little question that chromosomes in mitosis are metabolically
less active than those in interphase. Synthesis of D N A and R N A is
performed in interphase when the chromosomes are highly despiralized.
It may be logical to correlate the tightly condensed chromosomes with
the reduction of synthetic activities. Mitotic chromosomes resume their
physiological activity when they enter interphase; so that the inhibition
of synthesis is only temporary. Heterochromatin, however, remains
condensed in interphase. Would this then suggest that, whenever a
piece of chromatin retains its condensed or pyknotic state, it is physiologically less active or inactive? If so, the so-called "genetic inertness"
of heterochromatin may be only a reflection of metabolic inactivity,
not a priori the absence, of genes. T o substantiate the concept that
heterochromatic areas are metabolically less active, Hsu (1962)
selected a cell strain whose cells possessed a large number of heterochromatic blocks (chromocenters) in interphase to test, by means of
treatment with tritiated uridine, the capacity for R N A synthesis. As
can be seen from Fig. 12, R N A synthesis is distinctly more active in
areas outside the chromocente* s. This could mean that few or no
messengers can be sent out of the central post office for the cytoplasm
to receive specific information codes for making specific substances.
It must be added, however, that there is doubt that the heterochromatin remains condensed and is thereby metabolically inactive
throughout the cell cycle. No one really has observed a cell from one
mitosis to the next in respect of its chromocenter formation. That the
chromocenter in interphase represents the heterochromatic segment
which one sees in mitotic prophase is only deduced, not established
from direct tracing in living cells. Although it is true that correlation
has been established between prophase chromosomes and salivary
chromosomes, the salivary gland chromosomes are equivalent to
meiotic prophase, not interphase of somatic nuclei. Personally, I hvae
serious doubts that these two types of chromosomes are directly comparable in all respects, for we are not even certain about the methods of
DNA replication in the salivary cells. In pure speculation, the heterochromatin in the polytene system may not replicate as many times as
the euchromatin. Let us concede, however, that these two are the same.
439
were not; or both could be labeled; or the autosomes could be labeled
while the X remained unlabeled. This situation was similar to that of
the mitotic cells of the Chinese hamster just described. From all
reported cases it seems that chromosomes or chromosome parts, showing
heteropyknosis, synthesize D N A at the time when euchromatin has
completed its D N A replication. It is possible that the asynchronous
DNA synthesis is a direct consequence of the out-of-cycle coiling of
the chromosomes or chromosome parts which are heteropyknotic.
There is little question that chromosomes in mitosis are metabolically
less active than those in interphase. Synthesis of D N A and R N A is
performed in interphase when the chromosomes are highly despiralized.
It may be logical to correlate the tightly condensed chromosomes with
the reduction of synthetic activities. Mitotic chromosomes resume their
physiological activity when they enter interphase; so that the inhibition
of synthesis is only temporary. Heterochromatin, however, remains
condensed in interphase. Would this then suggest that, whenever a
piece of chromatin retains its condensed or pyknotic state, it is physiologically less active or inactive? If so, the so-called "genetic inertness"
of heterochromatin may be only a reflection of metabolic inactivity,
not a priori the absence, of genes. T o substantiate the concept that
heterochromatic areas are metabolically less active, Hsu (1962)
selected a cell strain whose cells possessed a large number of heterochromatic blocks (chromocenters) in interphase to test, by means of
treatment with tritiated uridine, the capacity for R N A synthesis. As
can be seen from Fig. 12, R N A synthesis is distinctly more active in
areas outside the chromocente* s. This could mean that few or no
messengers can be sent out of the central post office for the cytoplasm
to receive specific information codes for making specific substances.
It must be added, however, that there is doubt that the heterochromatin remains condensed and is thereby metabolically inactive
throughout the cell cycle. No one really has observed a cell from one
mitosis to the next in respect of its chromocenter formation. That the
chromocenter in interphase represents the heterochromatic segment
which one sees in mitotic prophase is only deduced, not established
from direct tracing in living cells. Although it is true that correlation
has been established between prophase chromosomes and salivary
chromosomes, the salivary gland chromosomes are equivalent to
meiotic prophase, not interphase of somatic nuclei. Personally, I hvae
serious doubts that these two types of chromosomes are directly comparable in all respects, for we are not even certain about the methods of
DNA replication in the salivary cells. In pure speculation, the heterochromatin in the polytene system may not replicate as many times as
the euchromatin. Let us concede, however, that these two are the same.