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CHARLES S. THORNTON
peated amputations. Verwoerd concluded that in the first series of experiments shielded mesenchymatous cells from the pelvic area and from
the nerve sheath in this region migrated to the limb tip where they
formed a blastema. Irradiation of the entire regeneration-competent area
removed this source of blastemal cells. It is possible that a similar
explanation can be applied to account for Polejaieff's results. Irradiation
of limb and pelvic area, with subsequent experimental trauma, should be
undertaken in order to settle this problem.
The origin of blastemal cells has been sought by other methods as well.
Chalkley (1954, 1959), in careful and detailed investigations of mitotic
patterns in regenerating newt limbs was able to correlate a large number
of mitoses with specific limb tissues in early regeneration stages. These
data provided him with an estimate of the extent of cellular contribution
by each stump tissue to the accumulation blastema but could not provide
evidence of tissue continuity throughout blastema proliferation and differentiation phases since it is not known whether the mitotic cycles of
blastemal cells are tissue specific or whether they may be influenced by
conditions unique to the regeneration blastema. Hay and Fischman
(1961) injected tritiated thymidine into regenerating newts 10 days after
limb amputation. Limbs were fixed at daily intervals thereafter, and the
dedifferentiating limb stump tissues were found to incorporate the label.
At 15 days the internal cells, which had incorporated tritiated thymidine
at 10 days, had given rise to labeled blastema cells thus indicating their
derivation from the dedifferentiating stump tissues.
Recently, Carlson (1967) has reported that limb regeneration in the
adult newt is inhibited by actinomycin D given 1 day before amputation.
Although wound healing and demolition are relatively little affected by
the antibiotic, tissue dedifferentiation is blocked. The resulting failure of
blastemal cells to accumulate is thus correlated with absence of stump
tissue dedifferentiation. Weber (1965) and Tata (1966) have shown that
actinomycin D inhibits the regression of tadpole tails after thyroxin
treatment. They conclude that protein synthesis is necessary for tail
regression. Indeed, Weber (1965) finds specifically a decrease in cathepsin activity in actinomycin D treated tails. Similar experiments have not
yet been done with the urodele limb (see Weiss and Rosenbaum, 1967,
however).
Although there is now considerable evidence that the blastemal cells
arise by the dedifferentiation of limb stump tissues, the question of
whether metaplasia normally occurs in regeneration has yet to be answered satisfactorily. The chief problem has been to identify cells at all
CHARLES S. THORNTON
peated amputations. Verwoerd concluded that in the first series of experiments shielded mesenchymatous cells from the pelvic area and from
the nerve sheath in this region migrated to the limb tip where they
formed a blastema. Irradiation of the entire regeneration-competent area
removed this source of blastemal cells. It is possible that a similar
explanation can be applied to account for Polejaieff's results. Irradiation
of limb and pelvic area, with subsequent experimental trauma, should be
undertaken in order to settle this problem.
The origin of blastemal cells has been sought by other methods as well.
Chalkley (1954, 1959), in careful and detailed investigations of mitotic
patterns in regenerating newt limbs was able to correlate a large number
of mitoses with specific limb tissues in early regeneration stages. These
data provided him with an estimate of the extent of cellular contribution
by each stump tissue to the accumulation blastema but could not provide
evidence of tissue continuity throughout blastema proliferation and differentiation phases since it is not known whether the mitotic cycles of
blastemal cells are tissue specific or whether they may be influenced by
conditions unique to the regeneration blastema. Hay and Fischman
(1961) injected tritiated thymidine into regenerating newts 10 days after
limb amputation. Limbs were fixed at daily intervals thereafter, and the
dedifferentiating limb stump tissues were found to incorporate the label.
At 15 days the internal cells, which had incorporated tritiated thymidine
at 10 days, had given rise to labeled blastema cells thus indicating their
derivation from the dedifferentiating stump tissues.
Recently, Carlson (1967) has reported that limb regeneration in the
adult newt is inhibited by actinomycin D given 1 day before amputation.
Although wound healing and demolition are relatively little affected by
the antibiotic, tissue dedifferentiation is blocked. The resulting failure of
blastemal cells to accumulate is thus correlated with absence of stump
tissue dedifferentiation. Weber (1965) and Tata (1966) have shown that
actinomycin D inhibits the regression of tadpole tails after thyroxin
treatment. They conclude that protein synthesis is necessary for tail
regression. Indeed, Weber (1965) finds specifically a decrease in cathepsin activity in actinomycin D treated tails. Similar experiments have not
yet been done with the urodele limb (see Weiss and Rosenbaum, 1967,
however).
Although there is now considerable evidence that the blastemal cells
arise by the dedifferentiation of limb stump tissues, the question of
whether metaplasia normally occurs in regeneration has yet to be answered satisfactorily. The chief problem has been to identify cells at all