MORPHOGENESIS OF CROWN
GALL
53
mind that TIP as such might even be nonexistent and that the results
obtained might be explicable on some other basis.
The location of the effective bacteria in the wounded tissue was
studied by Stonier (1956) who labeled the bacteria with
3 2
P and traced
them in the host tissue by means of autoradiography. His results suggest
that cell transformation is induced by the bacteria situated in the intercellular spaces. In his electron microscopic studies, Hohl (1961) confirmed the presence of bacteria in the intercellular spaces and, similarly,
Ryter and Manigault (1964) observed very few bacteria inside the living
cells. Also Rasch (1964) described the extracellular localization of the
crown gall organism. However, Gee et al. (1966, 1967) observed them
both in the host cells and in the intercellular spaces, although they disappeared at a later stage.
The earlier assumption that the number of the bacteria was not important in tumor formation has lately been shown to be incorrect. Beaud
and Manigault (1964) demonstrated that the tumor weight is the smaller,
the lower the concentration of the bacteria in the inoculum. Beaud
(1965) determined the amount of bacteria, of different strains, that was
needed to produce tumors of maximum weight in the stem of Datura
stramonium.
According to him, the weight of the galls was proportional
to the number of bacteria if this was smaller than 10
5 per wound. He
also stated that the number of bacteria increased in the wounded site,
but that the rate of the increase was dependent on the size of the original
inoculum.
Until recently, it had been generally accepted that the temperature at
which the alteration of normal cells to tumor cells can be accomplished
does not exceed 30°C. However, a report by J. A. Lippincott and B. B.
Lippincott (1966) throws some doubt on this belief. The authors studied
the effect of temperature on crown gall induction in pinto bean leaves. As
a rule, the tumor initiation was inhibited by temperatures of 32°C or
higher. In certain cases, however, temperatures of 32°-45°C even promoted tumor formation. This happened when, after the infection, the
plants were kept in the dark at 27°C for 72 hr and a 4-hr period of
elevated temperature was included in the first part of the dark period.
Maximum promotion was observed when the high-temperature treatment
was given at about 8 hr after infection, whereas a maximum inhibition
was caused at about 18 hr. Since a similar promotion in infectivity could
be achieved by subjecting bacteria to a 5-min treatment at 45°C prior
to inoculation, the authors suggested that the promotion of tumor formation might be due to the action of bacteria.
GALL
53
mind that TIP as such might even be nonexistent and that the results
obtained might be explicable on some other basis.
The location of the effective bacteria in the wounded tissue was
studied by Stonier (1956) who labeled the bacteria with
3 2
P and traced
them in the host tissue by means of autoradiography. His results suggest
that cell transformation is induced by the bacteria situated in the intercellular spaces. In his electron microscopic studies, Hohl (1961) confirmed the presence of bacteria in the intercellular spaces and, similarly,
Ryter and Manigault (1964) observed very few bacteria inside the living
cells. Also Rasch (1964) described the extracellular localization of the
crown gall organism. However, Gee et al. (1966, 1967) observed them
both in the host cells and in the intercellular spaces, although they disappeared at a later stage.
The earlier assumption that the number of the bacteria was not important in tumor formation has lately been shown to be incorrect. Beaud
and Manigault (1964) demonstrated that the tumor weight is the smaller,
the lower the concentration of the bacteria in the inoculum. Beaud
(1965) determined the amount of bacteria, of different strains, that was
needed to produce tumors of maximum weight in the stem of Datura
stramonium.
According to him, the weight of the galls was proportional
to the number of bacteria if this was smaller than 10
5 per wound. He
also stated that the number of bacteria increased in the wounded site,
but that the rate of the increase was dependent on the size of the original
inoculum.
Until recently, it had been generally accepted that the temperature at
which the alteration of normal cells to tumor cells can be accomplished
does not exceed 30°C. However, a report by J. A. Lippincott and B. B.
Lippincott (1966) throws some doubt on this belief. The authors studied
the effect of temperature on crown gall induction in pinto bean leaves. As
a rule, the tumor initiation was inhibited by temperatures of 32°C or
higher. In certain cases, however, temperatures of 32°-45°C even promoted tumor formation. This happened when, after the infection, the
plants were kept in the dark at 27°C for 72 hr and a 4-hr period of
elevated temperature was included in the first part of the dark period.
Maximum promotion was observed when the high-temperature treatment
was given at about 8 hr after infection, whereas a maximum inhibition
was caused at about 18 hr. Since a similar promotion in infectivity could
be achieved by subjecting bacteria to a 5-min treatment at 45°C prior
to inoculation, the authors suggested that the promotion of tumor formation might be due to the action of bacteria.