LINKAGE OF THE GENES FOR DDT AND DIELDRIN RESISTANCE IN LARVAE OF THE MOSQUITO AEDES AEGYPTI

1975 ◽  
Vol 17 (4) ◽  
pp. 543-551 ◽  
Author(s):  
Judith M. Hitchen ◽  
R. J. Wood

The DDT resistance gene RDDT1, and the dieldrin resistance gene Rd1 have been mapped on linkage group II with respect to visible markers, in the mosquito Aedes aegypti L. The best interpretation of the data gives the order wa – Rd1 – ds – RDDT1 – s – y but wa – Rd1 – ds – y – s – RDDT1 is also possible, h is very loosely linked with RDDT1. The length of the linkage group has been considerably extended from previous studies.

1970 ◽  
Vol 16 (1) ◽  
pp. 37-47 ◽  
Author(s):  
R. J. Wood

SUMMARYThe influence of the linkage group II locus y on DDT resistance in Aedes aegypti has been studied in crosses between the Trinidad resistant strain and QS susceptible strain. The y locus influences DDT resistance in both R/R and R/+ larvae. The effect of y may be interpreted as reducing the penetrance of R (RDDT1), which is also located on linkage group II. y+ is partially dominant and incompletely penetrant in its resistance-enhancing role (although in its pleiotropic effect on larval colour it is dominant and fully penetrant). Penetrance of y+ is influenced by an environmental factor, probably associated with the larval diet.The effect of y on resistance is evaluated in relation to other genetic influences on the expression of RDDT1.The significance of polymorphism at the y locus is discussed.


1975 ◽  
Vol 17 (3) ◽  
pp. 311-322 ◽  
Author(s):  
Judith M. Hitchen ◽  
R. J. Wood

The gene RDDT2, which gives resistance to DDT in the imago of Aedes aegypti L. has been mapped on linkage group III with respect to six visible markers. The best interpretation of the order of the genes is:–blp – blt – co – fz – wi – RDDT2 – min, but the orderblp – blt – co – fz – RDDT2 – wi – min is also possible.


1967 ◽  
Vol 10 (3) ◽  
pp. 219-228 ◽  
Author(s):  
R. J. Wood

Inheritance of DDT resistance has been studied in crosses between the highly resistant ‘T’ strain of A. aegypti (constituted by inbreeding from the TRINIDAD DDT-resistant stock) and the ‘64’ susceptible strain.Larval DDT resistance derives from a major gene RDDT1 on linkage group II, the order being RDDT1–s–y. Linkage group III may also contribute to larval resistance. Linkage group I makes no contribution.Adult DDT resistance derives from a major gene RDDT2, 18·2 ± 2·1 units from the market blt on linkage group III. Linkage group II has no influence on adult resistance.Selection with DDT to retain only RDDT1/+ segregants in larvae of backcrosses RDDT1/+×+/+ did not increase resistance in resulting adults, confirming the difference in genetic mechanism at the two stages.The F1 progenies from reciprocal crosses between ‘T’ and ‘64’ differed slightly but significantly in larval resistance, modifying the influence of the major gene RDDT1 in the heterozygote.The early developmental stages of the RDDT1/+ phenotype (up to the fourth larval stage) were more viable than the +/+ phenotype in backcross segregation. The difference in mortality probably exceeded 30%.


1970 ◽  
Vol 12 (3) ◽  
pp. 407-414 ◽  
Author(s):  
W. L. Lockhart ◽  
W. Klassen ◽  
A. W. A. Brown

Crosses and backcrosses between five dieldrin-resistant strains and the MYS susceptible strain in Aedes aegypti indicate the order of the genes to be Dl—si — s, the distance si — s being 6-7 units and the total distance Dl — s being 25-31 units.Crosses between the Trinidad DDT-resistant strain and the MYS marker strain indicate the order to be si — s — DDT, the distance si — s being 4 units and the total distance s — DDT being 10 units. Crosses between this strain and the AO and Multiple marker strains indicate the order to be y — s — DDT.These results indicate that the order of the genes in linkage-group 2 of Aedes aegypti is probably Dl — si — y —s — DDT. The total crossover distance of some 45 units thus implied between Dl and DDT is, however, at variance with previous work which found the direct crossover between these two genes to be only 4-7%.


1970 ◽  
Vol 15 (2) ◽  
pp. 227-235 ◽  
Author(s):  
A. G. Searle ◽  
Gillian M. Truslove

SUMMARYMice heterozygous for rump-white (Rw) have white hair in lumbo-sacral and caudal regions, although the tail-tip is sometimes pigmented. The homozygote is lethal in utero. No recombination has been found between Rw and the very closely linked spotting genes patch (Ph) and the viable allele of W (Wv). The compounds between these genes are all viable and fertile, although individual homozygotes are either lethal (Ph, Rw) or sterile and anaemic (Wv). It is concluded that they are non-allelic, but form a gene triplet. Close linkage between a cluster of dominant spotting genes and an angora gene in mouse and rabbit provide evidence for homology of part of linkage group II in the rabbit and part of linkage group XVII in the mouse.


1966 ◽  
Vol 8 (1) ◽  
pp. 111-113 ◽  
Author(s):  
D. S. Falconer ◽  
J. H. Isaacson

Curly-whiskers (cw) is a recessive gene which was found in 1958 by Mr C. J. W. Smith of the Chester Beatty Research Institute, London. It arose in a subline of the CBA/Cbi inbred strain. The first mutant animals were one male and one female in a litter of five. The two mutants were mated together and a sib-mated subline was continued from them in which 500 mice were bred, all of which were curly-whiskered. This established the mutant to be fully penetrant. Curly-whiskers resembles the hair-waving genes in causing waving of the vibrissae, but it has no obvious waving effect on the hairs of the coat. The coat texture is, however, slightly abnormal and Mr Smith noted also that on the CBA background there was an appreciable darkening of the coat colour. Homozygotes (cw/cw) are easily classifiable soon after birth by the curled vibrissae. Heterozygotes (+/cw) often have slightly curled vibrissae, and the gene is therefore not fully recessive; but the distinction between +/cw and +/+ could not be relied on, and in the linkage tests cw was treated as a recessive gene.


1963 ◽  
Vol 56 (4) ◽  
pp. 511-517 ◽  
Author(s):  
Z. H. Abedi ◽  
J. R. Duffy ◽  
A. W. A. Brown
Keyword(s):  

1961 ◽  
Vol 52 (6) ◽  
pp. 297-300 ◽  
Author(s):  
MARGARET C. GREEN
Keyword(s):  

Crop Science ◽  
2006 ◽  
Vol 46 (1) ◽  
pp. 168-173 ◽  
Author(s):  
Stuart G. Gordon ◽  
Steven K. St. Martin ◽  
Anne E. Dorrance

Genetics ◽  
1988 ◽  
Vol 118 (3) ◽  
pp. 425-436
Author(s):  
S C Kayman ◽  
R Birchman ◽  
M Clarke

Abstract The Dictyostelium discoideum mutant MC2 exhibits temperature-sensitive growth, temperature-sensitive motility, and temperature induction of discoidin I synthesis. These three phenotypes of MC2 were not separated in the genetic experiments reported here. They were therefore assigned to the mutation motA1552, which was mapped to linkage group II by segregation analysis and by analysis of mitotic recombinant diploids. In one motA1552 strain, loss of motility preceded accumulation of discoidin I by 3 hr, indicating that discoidin I is not involved in generation of the motility defect. Expression of motA1552 phenotypes varied both among strains carrying the mutation, and among different clones of a particular strain. MC2 and its derivatives displayed elevated levels of recombination between whiA and acrA on linkage group II, and yielded highly unstable mutations at the acrA locus. Accumulation of large amounts of discoidin I during axenic growth of strain AX3 was found to depend on the presence of a second linkage group II mutation, daxA1551. This mutation was already present in the strain mutagenized to isolate motA1552, complicating explication of motA1552 action.


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