MORPHOGENESIS OF CROWN
GALL
51
the latter question, i.e., the actual cell transformation, will be discussed
in the last section of this review. The assumptions concerning the nature
of the bacterial effect will be discussed below.
Braun and Stonier (1958) and Braun (1962) have reviewed the earlier
as well as the contemporary ideas concerning the bacterial effect. Braun
(1947) suggested that the factor causing the transformation could be
one of the following: (1) a metabolic product of the crown gall bacteria;
(2) a normal host constituent that is converted by the bacteria into a
tumor-inducing substance; (3) a chemical fraction of the bacterial cell;
(4) a virus or some other agent which is present in the crown gall
organism. As a fifth possibility Braun (1962) mentions that the bacteria
themselves might enter the wounded cells and become so altered that they
are no longer demonstrable. A series of experiments concerning the
effect of temperature on the infected plants led Braun to conclude that
the bacteria passed to the host cells some kind of factor that brought
about a complete and heritable change in the behavior of the cells. The
name "tumor-inducing principle" (TIP) was given to this hypothetical
factor, and it has been accepted into common usage. The nature of this
factor was and still is unknown. The experiments of Braun and Mandle
(1948) led them to conclude that the factor was thermolabile. They
suggested that TIP was cumulative or that the temperature of 32 °C
inactivated or destroyed it at the same rate as it was produced at 25°C.
The assumption of the thermolability of TIP was later questioned by
Lipetz (1965) who pointed out that in earlier studies not enough attention had been paid to the possible differences in the rate of the conditioning at different temperatures.
The possibility that TIP belongs to the nucleic acids, being some kind
of DNA, has been repeatedly proposed and experimentally tested since
Klein (1953) claimed that the amount of DNA increased more after
crown gall infection than after sterile wounding. This claim was proven
to be erroneous by Kupila and Stern (1961) who showed that, when
calculated as percentage of the DNA in healthy internodes, the amount
of DNA increased similarly both in the infected and in the sterile
wound tissue. The rate of the increase slowed down in a few days
so that the more steady replication of DNA in the healthy internodes helped it to reach the same quantitative level. Later, rapid cell
division in the crow
T
n gall tissue resulted in a considerable increase in the
amount of DNA as compared to the wounded tissue. The time at which
the increase in the rate of DNA formation occurred varied with tempera-
GALL
51
the latter question, i.e., the actual cell transformation, will be discussed
in the last section of this review. The assumptions concerning the nature
of the bacterial effect will be discussed below.
Braun and Stonier (1958) and Braun (1962) have reviewed the earlier
as well as the contemporary ideas concerning the bacterial effect. Braun
(1947) suggested that the factor causing the transformation could be
one of the following: (1) a metabolic product of the crown gall bacteria;
(2) a normal host constituent that is converted by the bacteria into a
tumor-inducing substance; (3) a chemical fraction of the bacterial cell;
(4) a virus or some other agent which is present in the crown gall
organism. As a fifth possibility Braun (1962) mentions that the bacteria
themselves might enter the wounded cells and become so altered that they
are no longer demonstrable. A series of experiments concerning the
effect of temperature on the infected plants led Braun to conclude that
the bacteria passed to the host cells some kind of factor that brought
about a complete and heritable change in the behavior of the cells. The
name "tumor-inducing principle" (TIP) was given to this hypothetical
factor, and it has been accepted into common usage. The nature of this
factor was and still is unknown. The experiments of Braun and Mandle
(1948) led them to conclude that the factor was thermolabile. They
suggested that TIP was cumulative or that the temperature of 32 °C
inactivated or destroyed it at the same rate as it was produced at 25°C.
The assumption of the thermolability of TIP was later questioned by
Lipetz (1965) who pointed out that in earlier studies not enough attention had been paid to the possible differences in the rate of the conditioning at different temperatures.
The possibility that TIP belongs to the nucleic acids, being some kind
of DNA, has been repeatedly proposed and experimentally tested since
Klein (1953) claimed that the amount of DNA increased more after
crown gall infection than after sterile wounding. This claim was proven
to be erroneous by Kupila and Stern (1961) who showed that, when
calculated as percentage of the DNA in healthy internodes, the amount
of DNA increased similarly both in the infected and in the sterile
wound tissue. The rate of the increase slowed down in a few days
so that the more steady replication of DNA in the healthy internodes helped it to reach the same quantitative level. Later, rapid cell
division in the crow
T
n gall tissue resulted in a considerable increase in the
amount of DNA as compared to the wounded tissue. The time at which
the increase in the rate of DNA formation occurred varied with tempera-