ANDROGENESIS, A DIFFERENTIATOR OF CYTOPLASMIC INJURY INDUCED BY X-RAYS IN HABROBRACON EGGS

¹ University of Pennsylvania

Wild type Habrobracon females were x-rayed and mated to untreated recessive males. Two kinds of haploid males were produced, gynogenetic (x-rayed chromosomes in x-rayed cytoplasm) and androgenetic (untreated chromosomes in x-rayed cytoplasm).

Eggs x-rayed in metaphase I x untreated sperm

Gynogenetic males develop from the unfertilized eggs, androgenetic males from fertilized. Death of the former and origin of the latter are caused by different degrees of the same type of x-ray induced chromosomal injury. Dose-hatchability curve for gynogenetic males is exponential and their lethal dose is that of the chromosomes in this stage, about 2400 r. Percentage of androgenetic males increases up to about 15,000 r, then gradually decreases until none is produced at about 54,000 r which is the lethal dose for the cytoplasm in this stage. Percentage of androgenetic males can be increased at doses above 15,000 r by fractionation.

Eggs x-rayed in prophase I x untreated sperm

Gynogenetic males develop from the unfertilized eggs. No androgenetic males develop due to absence of type of chromosome aberration necessary for their formation. Dose-hatchability curve for gynogenetic males is exponential up to about 15,000 r, after which it falls at an increased rate. It can be restored to an exponential curve by fractionating dose. Lethal dose is about 54,000 r. This is the lethal dose for cytoplasm. That for the chromosomes in this stage is considerably higher.

Chromosomal vs. cytoplasmic injury

Some androgenetic males survive after dose over twenty times greater than that which is lethal for chromosomes of eggs in which they develop. At all doses they resemble the controls and differ significantly from gynogenetic males in visible mutation rate, viability, and fertility. The changes peculiar to gynogenetic males must be chromosomal in origin since both types of males develop in irradiated cytoplasm. Evidence suggests that these changes are directly induced and supports the target theory of chromosomal injury.

Since there is no evidence for chromosomal injury in surviving androgenetic males, the reduction of their number at doses above 15,000 r, through embryonic death, must be directly cytoplasmic.

The increase in survival of both gynogenetic and androgenetic males in response to fractionation of dose must be due to reduction of cytoplasmic injury since they have only x-rayed cytoplasm in common.

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