1022-7954/04/4005- © 2004
Russian Journal of Genetics, Vol. 40, No. 5, 2004, pp. 500–505. Translated from Genetika, Vol. 40, No. 5, 2004, pp. 624–630.
Original Russian Text Copyright © 2004 by Vasilyeva, Ratner.
Genetics of quantitative characters is a traditional
but one of the most complex ﬁelds of classical genetic
analysis. Despite undisputable advances, this area of
research is substantially behind other genetic ﬁelds in
understanding genetic determination, ontogenetic path-
ways of their formation, their population dynamics, and
mechanisms underlying artiﬁcial selection and evolu-
tion of quantitative characters.
Classical studies of Johannsen , Nilsson-Ehle ,
Mather , Mather and Jinks , Thoday , Falconer
, and other authors have developed the following
views on inheritance of quantitative characters.
(1) These characters are inherited according to the
(2) Each quantitative character is controlled by a
several (or many) genetic factors. Acting cumulatively,
these factors create genetic variability of the character.
(3) The environment is also variable and consider-
ably affect the formation of quantitative characters.
(4) Continuous phenotypic variation of quantitative
characters is explained by the effects of many genes and
Genetic statistical models of Wright  and Fisher ,
which had been developed to evaluate the genetic compo-
nent of phenotypic variance in quantitative characters, for
several reasons produced a very approximate estimate of
this parameter. First, these models described a special case
of a character controlled by one gene with two alleles; sec-
ond, environmental ﬂuctuations were neglected; and,
third, intralocus (dominance) and interlocus (epistasis)
gene interactions were not considered.
These one-locus models were extrapolated to the
cases of polygenic control of quantitative characters.
Proposing to use the one-locus model for analysis of
quantitative characters, Lush  made a number of
assumptions: quantitative characters are controlled by
many genes with small, equal, and additive contribu-
tions; the environment is stable; coefﬁcient of correla-
tion between the parental genotype and phenotype is
equal to the corresponding coefﬁcient of correlation in
However, many experiments yield data that do not
allow to describe genetic control of quantitative charac-
ters within the framework of the models proposed by
Wright and Fisher.
In the present study, we demonstrate the complexity of
genetic control of such characters using a simple quantita-
tive character, the radial wing vein L2 of
As characters, we consider sizes of the proximal (px)
and distal (dt) fragments of the longitudinal wing vein,
whose formation is controlled by recessive mutation
chromosome 3, 47.0 cM).
In the process of development, the longitudinal
veins (coxal L1, radial L2, medial L3, cubital L4, and
anal L5) are ﬁrst seen on the wings of
as longitudinal protrusions having more dense cuticular
structure than the remaining wing surface. These pro-
trusions are visible on both dorsal and ventral sides of
the wings. Garsia-Bellido  has shown that veins L3,
L5, and the tip of L4 are dorsal protrusions whereas L2
is mostly ventral. The process of vein formation contin-
ues at the pupal stage. When the dorsal and ventral
wing blades are joined, the vein formation is com-
pleted. Mature veins are seen as hollows on the dorsal
and ventral wing surfaces. In wild-type ﬂies, veins lack
bristles (except those on the edge of L1). According to
Analysis of the Expression System of Gene
L. A. Vasilyeva
and V. A. Ratner
Institute of Cytology and Genetics, Russian Academy of Sciences, Novosibirsk, 630090 Russia;
fax: (3832) 33-12-78; e-mail: email@example.com
Novosibirsk State University, Department of Cytology and Genetics, Novosibisrsk, 630090 Russia
Received June 4, 2003
—The genetic expression system of gene
was studied by substituting regions of
chromosome 3 from line
th st ri sr ca
, which has drastically reduced
expression, to regions of chromosome
3 from a “selection” line
having very high expression of this gene. Virtually all chromosome 3 was shown
to carry polygenes controlling phenotypic expression of oligogenic mutation
Chromosome regions making
large (as well as small and even negative) contributions to sizes of the distal and proximal fragments of the lat-
itudinal wing vein were found. These results suggest that the genetic system of expression does not correspond
to the generally accepted postulates of K. Mather on equal, small, and additive contributions of polygenes.