1022-7954/02/3810- $27.00 © 2002
Russian Journal of Genetics, Vol. 38, No. 10, 2002, pp. 1145–1149. Translated from Genetika, Vol. 38, No. 10, 2002, pp. 1351–1356.
Original Russian Text Copyright © 2002 by Ivashchenko, Grishaeva.
Extensive evidence has been currently accumulated
suggesting that mechanisms underlying chromosome
damage caused by irradiation and transposition of
mobile elements (ME) are somewhat similar. In both
cases, the double-stranded DNA breaks appear and the
break points are irregularly distributed along a chromo-
some [1–3]. Some authors suggest that the break for-
mation induced by either irradiation or ME activity
triggers the recombination repair system analogous to
that responsible for the SOS response in bacteria and
the DNA synthesis is determined by the template and
the enzyme activity .
To date, it is beyond doubt that ME transposition
induces most spontaneous mutations. Outbreaks of
general and gene-speciﬁc species mutability observed
during some historical periods are currently discussed
in light of these new scientiﬁc advances. An ability of
the mobile genetic elements to become active under
speciﬁc conditions may account for the aforementioned
events. In some cases, ME transpositions are induced
by a system of crosses, the so-called hybrid dysgenesis
(HD); in other cases, by temperature. Limited evidence
on the effect of active chemical compounds and irradi-
ation on ME transposition is available [5,6].
, the development
of HD systems observed in the last 40–50 years is
assumed to be induced by increasing environmental
pollution by chemical and radioactive wastes. These
systems are characterized by high genetic susceptibility
and sterility caused by transposition of MEs from two
. The latter are structurally and
functionally heterogeneous, because they include both
full-sized (active) and truncated (deleted) forms,
which, along with the cell cytotype, control transposi-
tion of mobile genetic elements in HD systems. The
expression of hybrid dysgenesis traits depends on the
interaction between the cell nucleus and cytoplasm, i.e.,
under conditions of a deﬁnite cytotype .
The objective of this work is studying the processes
induced by irradiation and ME transposition in the P–M
and H–E systems of HD as well as hybrid viability at
both embryonic and postembryonic developmental
stages. The frequencies of polytene chromosome rear-
rangements in third instar larvae and the recombination
frequencies were also estimated.
MATERIALS AND METHODS
Lines of Drosophila melanogaster used in the study
) was isolated by Green  from a nat-
ural population in 1975. It carries an inversion (cross-
over suppressor) marked with an additional mutation
and some recessive mutations:
The line has Q and H cytotypes.
y w ct
) is a
laboratory line obtained by T. I. Gerasimova , which
carries the following morphological markers:
. The line has
M' and E cytotypes.
(3) Line Domodedovskaya-18 (D18) was isolated
by T.A. Toropanova from a natural population in 1953.
The D18 line has M E cytotype (our unpublished data).
strong P-line carrying P cytotype was isolated
by Engels from a natural population .
Characteristic Features of Induced Mutagenesis
in Hybrid Dysgenesis Systems of
N. I. Ivashchenko and T. M. Grishaeva
Vavilov Institute of General Genetics, Russian Academy of Sciences, Moscow, 119991 Russia;
Received January 21, 2002
—The mutagenic effect of low-dose gamma-irradiation was studied in
tems of hybrid dysgenesis by estimating polytene chromosome rearrangements, recombination frequency, and
viability at the embryonic and postembryonic developmental stages. A dose of gamma-irradiation which had
no effect detectable by routine interstrain cross proved to signiﬁcantly reduce the number of recombinants in
the H–E and P–M systems and mortality at postembryonic stages. However, this combined effect was obtained
if irradiation followed trasposition, i.e., it depended on the application sequence of the mutagenic factors. The
reverse order of the mutagenic treatment led to summation of the effects: as compared to either control, the fre-
quencies of the dominant lethal mutations as well as the larval and pupal mortality in F
(at the level of 99.9%). This allowed us to estimate the contribution of extremely low-dose gamma-irradiation
into the mutagenic effect, which was impossible under routine conditions.