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Chromosomal assignment of the genetic factor, tu-91k,
responsible for a melanotic tumour in the Drosophila
melanogaster adult female
K Kosuda
To cite this version:
Note
Chromosomal
assignment
of the
genetic factor, tu-91k, responsible
for
a
melanotic
tumour
in
the
Drosophila
melanogaster
adult
female
K
Kosuda
Josai
University, Faculty of Science, Biological
Laboratory,
Sakado,
Saitaraa350-02, Japan
(Received
3 March1992; accepted
5August
1992)
Summary - Chromosomal transfer
experiments
were carried out toassign tu-91k,
thegenetic
factorresponsible
for theorgan-specific
and female-limited adult melanotic tumourin
Drosophila melanogaster.
It was found that the second chromosome has apredominant
effect and tu-91k is semidominant in its
phenotypic expression.
melanotic tumour
/
Drosophila melanogaster/
chromosomeassignment
/
semi-dominanceRésumé - Assignation chromosomique du facteur génétique tu-91k, responsable du
développement d’une tumeur mélanique chez la femelle de Drosophila melanogaster.
Des
expériences
detransfert chromosomique
ont été réalisées en vued’assigner
le facteur
génétique tu-91k, responsable
d’une tumeurmélanique spécifique
d’un organe et limitée à lafemelle
adulte deDrosophila melanogaster.
Il a été trouvé que le deuxième chromosome a uneffet prédominant
et que tu-91k est semi-dominant dans sonezpression
phénotypique.
tumeurmélanique
/
Drosophila melanogaster/
assignation chromosomique/
semi-dominanceINTRODUCTION
Many
different melanotic tumour strains have been described inDrosophila
and other insects sinceBridges
(1916)
firstreported
one inDrosophila melanogaster,
butonly
in a rather smallportion
have the tumour genes beenanalysed
in detail(Gateff
low
penetrance.
Inprevious
papers, Kosuda(1990, 1991)
reported
a new melanotictumour
strain,
C-104,
in Dmelanogaster,
in which thepenetrance
is ratherhigh.
The tumour in the C-104 strain has severalunique
characteristics(Kosuda, 1991).
As this melanotic tumour
develops
at an adultstage,
whereas most other tumours appear in larvalstages,
especially
in the 3rd instar larvaeshortly
beforepupation,
this tumour can be classified as an adult one. It can
only
be detected under themicroscope
in femaleflies, especially
in thevicinity
of thespermathecae.
In otherwords,
itsexpression
is sex-limited andorgan-specific.
Tumours often becomemacroscopically
visible as dense black bodies within the abdominalcavity
whenthey fully
develop.
The incidence of tumourdevelopment
was shown to increase with age (Kosuda, 1990). To test the role ofmajor
chromosomes of Dmelanogaster
in thedevelopment
of melanotictumours,
chromosomal transferexperiments
werecarried out in the
present
study.
MATERIALS AND METHODS
The melanotic tumour strain
C-104,
used in thisstudy
is ahighly
inbred one and isderived from a natural
population
inBudapest, Hungary.
The 2major
autosomesand the X chromosome of the C-104 strain were
independently
madehomozygous
by
a routineprocedure utilizing
&dquo;balancer&dquo; chromosomes.Complicated
inversions contained in these balancer chromosomesprevent
re-combination between the
homologous
chromosomes,
and thus preserve theoriginal
genetic
content of the chromosome in the C-104 strain. Second and thirdchromo-somes were marked with
Cy
In(2LR) CyL/Prrc
and with In(3LR)
TM3!76a;/6’6,
respectively.
The sex chromosome was also marked with the Muller-5 chromosome.The
mating
scheme ispresented
infigure
1. Female flieshomozygous
forrespective
chromosomes were maintained for 2 wk at 29°C to facilitate
ageing, by
transferring
these flies to fresh vials
containing
standard cornmealyeast
media every 2 or 3 d. After 2wk,
female flies weresingly
dissected inRinger
solution forDrosophila
underthe
microscope
and were examined under themicroscope
for presence or absenceof melanotic tumours in the
vicinity
of bothspermathecae
(figs 2a,b,c).
RESULTS AND DISCUSSION
Numerical results are
given
in table I. Theprincipal genetic
factorcausing
melanotictumours in the
aged
females is located on the secondchromosome,
as isexplicitly
shown in table I.
The
genetic
factorresponsible
for thedevelopment
of femalespecific
melanotic tumours in the C-104 strain isdesignated
tu!-91k. The 3rd chromosome and X chromosome areapparently
not involved in theexpression
of the melanotic tumourdevelopment
in the C-104 strain. It ispossible
that modifier loci are involved on other than the secondchromosome,
as thegenetic
control of other melanotictumours has
generally
been found to be multifactorial(Barigozzi
etal 1960;
Burnet andSang,
1964;
Mampell,
1967;
Lindsley
andGrell,
1968;
Belt andBurnet, 1972;
Sparrow,
1974,
1978).
It seems evident that the presence of a second chromosomethe
proportion
of fliescarrying
melanotic tumours among thosehomozygous
for the second chromosome is not less than that in theoriginal
C-104 strain asreported
inKosuda
(1990),
although
reduction in thephenotypic
expression
isusually expected
in such crossesowing
tochanges
in thegenetic background.
The
heterozygous
effect of tu-91k on theexpression
of thisorgan-specific
andfemale-limited adult melanotic tumour was also studied
using
3-wk-old femaleflies. The tu-91k
heterozygous
females were obtainedby
crosses between theC-104 strain and
Cy
In(2LR)CyL
Pm or Carton - S strain. The resultsare
summarized in table II. Ratios I and II
showing
theproportion
of melanotictumour-developing
females orspermathecae
inheterozygous
females are 0.179 and 0.095 onthe average,
respectively.
On the otherhand,
ratios I and II inhomozygotes
are0.281 and
0.186,
respectively.
Since thesefigures
inheterozygous
females are almosthalf of those in
homozygotes,
tu-91k seems to be semi-dominant. In otherwords,
thedegree
of dominance(h)
seems to benearly
0.5.The
present
results confirm that the melanotic tumourdevelopment
in theC-104 strain of D
melanogaster
isgenetically
controlled and thehereditary
mode isrelatively simple
and the second chromosome has apredominant
effect. Themajor
gene
responsible
for this melanotic tumour mutation on the second chromosome isnamed tu-91k. It should be noted that the tu-91k gene is not recessive as are other
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