Repair studies utilizing a fly-pupariation model of postmitotic cell response.
Delay in pupariation of irradiated fly (and other insect) larvae results from a neuroendocrine disturbance and represents a dose-dependent response of differentiated postmitotic tissue. Many experimental manipulations (e.g. heating) may themselves upset timing, limiting usefulness of this phenomenon as a model of postmitotic tissue response. Doses greater than 20 Gy inhibit retraction of specific muscles at time of pupariation, leading to formation of elongate puparia. Degree of elongation (ratio of length: breadth) was also a function of dose. Peak sensitivity for elongation occurs later than that for delay, but both endpoints exhibit rapid kinetics for sparing effect of dose fractionations (sdf). With degree of elongation as endpoint, we demonstrated synergism between heat and radiation, and heat markedly inhibited sdf. Maintenance of irradiated larvae under wet conditions greatly prolonged the larval stage, and degree of elongation was reduced. This recovery, analogous to repair of potentially-lethal damage (PLD) in plateau-phase cell cultures, proceeds much more slowly than sdf.
D000818:Animals; D004175:Diptera / Q000254:growth & development / Q000528:radiation effects*; D004307:Dose-Response Relationship, Radiation; D006358:Hot Temperature; D008938:Mitosis; D011679:Pupa / Q000528:radiation effects; D013997:Time Factors