1022-7954/05/4103- © 2005 Pleiades Publishing, Inc.
Russian Journal of Genetics, Vol. 41, No. 3, 2005, pp. 237–243. Translated from Genetika, Vol. 41, No. 3, 2005, pp. 312–319.
Original Russian Text Copyright © 2005 by Lebedeva, Trunova, Omelyanchuk.
A system of adaptive response permanently func-
tions in living cells. During the ongoing mitotic cycle,
stochastic and induced errors that disturb functioning
of intracellular structures can be corrected through
DNA repair , checkpoint system , the mechanism
of cryptic accumulation of variation , proteins con-
trolling processing of the mutant protein, protein iso-
forms, proteins with an overlapping (“redundant”)
function , etc.
In some mutant strains of
characterized by an altered structure of mitotic chromo-
somes, we  and a number of other authors  have
observed cellular adaptive modiﬁcation, which mani-
fested only in distant generations. Mechanisms of such
adaptive processes are unclear and received only spec-
ulative explanations. It was proposed that the lost func-
tion might be restored on the basis of structural and
functional heterochromatin plasticity regulated by
numerous genes . According to this assumption, dur-
ing the prolonged maintenance of the mutant strain,
trans-acting factors normalizing the expression of the
mutant genes are ﬁxed in the culture.
The appearance of mitosis tolerance to mutation
effects and the subsequent cell selection may occur in
the process of the so-called adaptive mutagenesis
(hypermutagenesis), which was described for prokary-
otes [3, 7] and assumed for eukaryotes .
In the present work, we describe a decrease in fre-
quency of some mitosis abnormalities in distant gener-
ations of mutant
gene product, protein cyclin B (CycB),
is one of the key elements of the cell cycle machinery
providing progressive cell movement through mitotic
cycle. As a part of the complex protein MPF (matura-
tion promoting factor), cyclin B is involved in major
mitotic events. The function of this protein is related to
regulation of the activity of a major mitotic protein
kinase, cyclin-dependent kinase 1 (Cdk1), and possibly
with determination of the speciﬁc subcellular localiza-
tion of this kinase and Aurora B. Cdk1 activation is a
multi-step process, which begins with cyclin B attach-
ing to kinase. The resultant complex CycB/Cdk1 does
not yet show catalytic activity. However, in the MPF
complex, the conformational state of the Cdk1 subunit is
changed in such a way that its functional sites become
accessible for a series of consecutive reactions of phos-
phorylation/dephosphorylation, through which the cat-
alytic subunit is activated. The activated CycB/Cdk1
complex phosphorylates mitotic proteins that are sig-
niﬁcant for formation and functioning of the mitotic
spindle and reorganization of the interphase chromatin
in mitotic chromosomes.
, two group B cyclins have been
found, CycB and CycB3 . It is thought that CycB is
involved in the mitotic spindle formation and CycB3, in
chromosome condensation. Both cyclins affect fertility.
CycB destruction at the exit from mitosis is signiﬁcant
for anaphase B and cytokinesis .
gene is mapped to region 58F-59A of
chromosome 2 in
In our laboratory,
we obtained mutation
insertion into this gene, which was established from the
results of cloning of the genomic DNA adjacent to the
is one of the ﬁrst major mutations
gene that decreases viability of homozygotes
and induces sterility in both sexes [11, 12]. In what fol-
lows, we present the results of studying cytological
effects of this mutation. It was shown that
to defective chromosome condensation and segrega-
tion. During the three-year period of maintenance of
the mutation in heterozygote, frequencies of some
defects decreased via cellular adaptive modiﬁcation.
The possible nature of the abnormalities and mecha-
nisms of their correction are discussed.
Genetics of the Cell Cycle: Adaptive Modification
Mutation Expression in Dividing Cells
L. I. Lebedeva, S. A. Trunova, and L. V. Omelyanchuk
Institute of Cytology and Genetics, Russian Academy of Sciences, Novosibisrsk, 630090 Russia;
fax: (3828) 33-13-78, e-mail: firstname.lastname@example.org
Received March 22, 2004; in ﬁnal form, June 30, 2004
—The effect of mutation
on mitosis in neural ganglia and imaginal disks was studied in third-
instar larvae of
. Chromosome condensation and segregation were shown to be
impaired in dividing cells of mutant larvae. During the three-year period of maintenance of the mutation in het-
erozygote, frequencies of some defects decreased via cellular adaptive modiﬁcation.