ISSN 1022-7954, Russian Journal of Genetics, 2008, Vol. 44, No. 9, pp. 1054–1060. © Pleiades Publishing, Inc., 2008.
Original Russian Text © V.L. Chubykin, 2008, published in Genetika, 2008, Vol. 44, No. 9, pp. 1209–1215.
1054
INTRODUCTION
It is known that mutations mainly impair the func-
tions of gene products, and the majority of products to
a certain degree influence the viability of progeny.
Selection eliminates the lethal mutations, while the
mutations with a weak effect are preserved (as they are
lethal for only part of the progenies) and even can be
accumulated. Timofeeff-Ressovsky called these muta-
tions minor physiological mutations (as they did not
appear morphologically) [1]; however, the commonly
accepted term now is deleterious mutations not only
due to their negative effect on viability, but also because
they interfere with the accumulation of favorable muta-
tions and, consequently, slow down the progressive adap-
tive evolution. It is assumed that sexual reproduction is a
tool for active elimination of deleterious mutations during
meiosis [2–6], which was the particular factor for its evo-
lutionary emergence and wide abundance.
An important argument in favor of such opinion is
the methodology of study and accumulation of delete-
rious mutations by disturbing main meiotic processes.
The idea and technique for accumulation and recording
of mutations belongs to Muller [7] and involves sup-
pression of chromosome pairing and recombination
over many generations. This is achieved by selection
for further reproduction in each generation of the het-
erozygotes at the chromosome studied with the so-
called balancers, the tools preventing crossing over,
which carry numerous inversions of chromosome
regions lethal in homozygotes. The experiments on
mutation accumulation in
Drosophila
for 20–40–100
generations (experiment durations, from 1 to 5 years)
have been reported [7–10]. In these cases, the survival
rate of progenies is decreased by only several percent.
Both the nature of these mutations and their interaction
pattern during accumulation in the genome are still
unknown. Presumably, the answer to this question
requires longer-term experiments with more significant
characteristics. The problem of studying the recombi-
nation suppression over hundreds and several thou-
sands of generations on the survival rate of
Drosophila
progenies requires a new experiment approach. Our
approach involves studying the survivability of the
progenies in the known laboratory strains carrying mei-
otic mutations from the world
D. melanogaster
collec-
tion maintained using balancer chromosomes. Meiosis
in such strains is abnormal not only in the heterozy-
gotes, but also in the homozygotes at meiotic muta-
tions. In this work, we continued the study of deleteri-
ous mutations accumulated in various strains carrying
mutation
c(3)G
[6].
MATERIALS AND METHODS
The following
Drosophila
melanogaster
strains
were used in the work:
(1) wild type (Oregon R) (+);
(2)
st
[1]
c
(3)
G
[1]
ca
[1]/
TM
2
ri
Ubx
[130]
e
[
s
]
ca
[1]
(
c
(3)
G
/
Ubx
)
;
(3)
st
[1]
c
(3)
G
[1]
ca
[1]/
TM
3
y
+
ri
[1]
p
[
p
]
sep
bx
[34
e
]
e
[
s
]
Sb
[
sbd
-1]
Ser
[1]
(
c
(3)
G
/
TM
3)
;
(4)
sp
[2]
st
[1]
c
(3)
G
[1]
ca
[1]/
TM
1
Me
[1]
kni
[
ri
-1]
Sb
[
sbd
-1]
(
c
(3)
G
/
TM
1)
;
(5)
ru
[1]
h
[1]
th
[1]
st
[1]
cu
[1]
sr
[1]
e
[
s
]
ca
[1]
;
Deleterious Mutations in Various
Drosophila melanogaster
Strains Carrying Meiotic Mutation
c(3)G
V. L. Chubykin
Vavilov Institute of General Genetics, Russian Academy of Sciences, Moscow, 119991 Russia;
e-mail: chubykin@vigg.ru
Received April 24, 2007
Abstract
—In the absence of meiotic recombination, deleterious mutations, decreasing the viability, are accu-
mulated and fixed in small
Drosophil
a populations. Study of the viability of hybrid progenies of three labora-
tory
Drosophila melanogaster
strains carrying meiotic mutation
c(3)G
17
has suggested that the deleterious
mutations are negatively synergistic in their interaction. The deleterious mutations localized to the pericentro-
meric region of chromosome 3 are threefold more efficient as compared with the mutations located in distal
regions. Substitution of a new chromosome for the balancer chromosome in a strain with meiotic mutation
c(3)G
17
partially restores (by ~20%) the viability of homozygotes
c(3)G
17
/c(3)G
17
over the first 20–30 genera-
tions. Further cultivation for 30 generations with the same balancer again decreases the viability to the initial
level. An epigenetic nature of deleterious mutations is discussed.
DOI:
10.1134/S102279540809007X
GENERAL
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