1022-7954/03/3905- $25.00 © 2003
Russian Journal of Genetics, Vol. 39, No. 5, 2003, pp. 592–595. Translated from Genetika, Vol. 39, No. 5, 2003, pp. 717–720.
Original Russian Text Copyright © 2003 by Vasilyeva, Ratner, Antonenko, Lopukhova, Bubenshchikova.
In our previous studies, we presented ample data on
MGE transposition induction by different stressful
external (heat shock, cold shock, heavy heat shock,
irradiation [1–4] and genetic (isogenization, inbreed-
ing, outbreeding ) factors. In many of these cases,
the molecular mechanism of induction is based on the
system of the genomic response to heat shock (HS) 
although other mechanisms cannot be excluded.
Detailed examination of the HS system [1, 6] has
shown that it is not a narrow specialized but a general-
ized genomic system capable of induction by a wide
variety of physical, chemical, and biological factors:
temperature, poisons, detergents, heavy metal ions,
, injection of denatured protein, viral infection, etc.
It is believed that the direct effect of the HS system is
associated with elimination of conformational defects
of proteins (operation of chaperones) regardless of the
origin of these defects. All factors producing such
defects can serve as inductors of the HS system.
In this perspective, MGE transposition induction by
HS system factors seems to be a side effect connected
to characteristics of the MGE molecular structure, in
particular, the presence of functional sites of the HS
system involved in induction. Motifs of these sites were
in fact found in sequenced regions of retrotransposons,
element, and other MGEs . However, no direct
experimental evidence of their function has been
obtained so far.
Notwithstanding, nothing prevented us from show-
ing experimentally whether MGE transposition (indi-
rectly using the HS system) can be induced by other
factors listed above, in particular, ethanol. Clearly, in
addition to the narrow focus of the experiment, this fac-
tor is of special interest from the viewpoint of mass
alcohol consumption and its possible genetic conse-
quences in humans.
In the present study, we present the ﬁrst data on the
inducing role of ethanol on MGE transposition in an
isogenic strain of
These results were pre-
sented in a brief form in abstracts of a scientiﬁc confer-
ence , report sessions and poster session of the Aca-
demic Council of the Institute of Cytology and Genet-
ics (February 2002).
Isogenic strain 51.
In our experiments we used
isogenic strain 51 of
the Mendelian mutation
was created by isogenization in 1991 and repeatedly
used in our studies of transposition induction [1, 2, 4].
During 10 years strain 51 stably maintained the
pattern containing 32 copies of this element.
The sum of fragment lengths of the longitudinal wing
vein induced by the
mutation is a
convenient quantitative trait: the strain readily responds
to inducing factors, and in case of induced genetic vari-
ability, also to selection on the quantitative trait
MGE transposition induction by ethanol fumes.
A pure vial without nutrient medium at 25
plugged with a glass pipette having a reservoir for liq-
uid. The reservoir contained a piece of cotton wool
abundantly wetted with ethanol. Ethanol fumes entered
the vial by the pipette channel. After the establishment
Induction of MGE
Transposition in an Isogenic Strain
by Different Doses of Ethanol Fumes
L. A. Vasilyeva
, V. A. Ratner
, O. V. Antonenko
E. D. Lopukhova
, and E. V. Bubenshchikova
Institute of Cytology and Genetics, Russian Academy of Sciences, Novosibirsk, 630090 Russia;
fax: (3832) 33-12-78; e-mail: firstname.lastname@example.org
Department of Cytology and Genetics, Novosibirsk State University, Novosibirsk, 630090 Russia
Received May 27, 2002
—The effect of treatment of males from an isogenic
strain by limiting doses
of ethanol fumes on transpositions of MGE
was examined. Validity of the phenomenon of transposition
induction was demonstrated. We estimated rates of induced transposition (
events per site, per sperm, per
in control) and showed dose dependence of the rate on the exposure time of the males
to ethanol fumes. Experiments with alcohol treatment at limiting doses must end either in death of the individ-
uals or bursts of genetic variability in their progeny. In terms of genetics of an individual, this may mean loss
of vital hereditary basis followed by mass degradation of the progeny of the “hard drinkers.” In terms of popu-
lations genetics, this mode of MGE transposition induction can rapidly create a burst of novel genetic variation,
which, apart of great losses, may generate a number of advantageous individuals, i.e., be signiﬁcant for popu-
lation survival in new, stressful environments.