scholarly journals Curly-whiskers and its linkage with tail-kinks in linkage group II of the mouse

1966 ◽  
Vol 8 (1) ◽  
pp. 111-113 ◽  
Author(s):  
D. S. Falconer ◽  
J. H. Isaacson
Keyword(s):  
Linkage Group ◽  
Inbred Strain ◽  
Recessive Gene ◽  
Coat Colour ◽  
Group Ii ◽  
Research Institute

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.

scholarly journals Snell's waltzer, a new mutation affecting behaviour and the inner ear in the mouse

1966 ◽  
Vol 8 (3) ◽  
pp. 339-345 ◽  
Author(s):  
M. S. Deol ◽  
Margaret C. Green
Keyword(s):  
Linkage Group ◽  
Inner Ear ◽  
Organ Of Corti ◽  
Recessive Gene ◽  
New Mutation ◽  
Group Ii

A new recessive gene affecting behaviour and the inner ear in the mouse has been discovered. It was named Snell's waltzer, and assigned the symbol sv. It is in linkage group II, about two map units from short ear (se) on the side opposite to that of luxoid (lu). The behaviour of sv/sv mice closely resembles that of other members of the shaker-waltzer group. The abnormalities of the inner ear consist in degeneration of certain parts following normal morphogenesis. The entire neuro-epithelium —that is, the organ of Corti, the two maculae and the three cristae—is affected, and this feature distinguishes it from other degenerative type mutants of this group.

scholarly journals Muted, a new mutant affecting coat colour and otoliths of the mouse, and its position in linkage group XIV

1969 ◽  
Vol 14 (2) ◽  
pp. 163-166 ◽  
Author(s):  
Mary F. Lyon ◽  
R. Meredith
Keyword(s):  
Linkage Group ◽  
Autosomal Recessive ◽  
Recessive Gene ◽  
Coat Colour ◽  
Group Xiv ◽  
Eye Colour ◽  
Autosomal Recessive Gene

The autosomal recessive gene muted, mu, which arose spontaneously, dilutes coat and eye colour and causes absence of otoliths in some but not all homozygotes. Its locus is in linkage group XIV of the mouse, and the order of loci was shown to be bg–Xt–sa–mu–f–pe.

scholarly journals A gene triplet in the mouse

1970 ◽  
Vol 15 (2) ◽  
pp. 227-235 ◽  
Author(s):  
A. G. Searle ◽  
Gillian M. Truslove
Keyword(s):  
Linkage Group ◽  
In Utero ◽  
White Hair ◽  
Close Linkage ◽  
Group Ii ◽  
Tail Tip ◽  
Dominant Spotting

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.

Mapping genes for resistance to Leptosphaeria maculans in Brassica juncea

Genome ◽  
2006 ◽  
Vol 49 (1) ◽  
pp. 30-41 ◽  
Author(s):  
J A Christianson ◽  
S R Rimmer ◽  
A G Good ◽  
D J Lydiate
Keyword(s):  
Linkage Group ◽  
Brassica Juncea ◽  
Fragment Length Polymorphism ◽  
Leptosphaeria Maculans ◽  
Recessive Gene ◽  
Brassica Species ◽  
Blackleg Disease ◽  
Recessive Resistance ◽  
B Genome ◽  
Restriction Fragment Length

Blackleg disease of crucifers, caused by the fungus Leptosphaeria maculans, is a major concern to oilseed rape producers worldwide. Brassica species containing the B genome have high levels of resistance to blackleg. Brassica juncea F2 and first-backcross (B1) populations segregating for resistance to a PG2 isolate of L. maculans were created. Segregation for resistance to L. maculans in these populations suggested that resistance was controlled by two independent genes, one dominant and one recessive in nature. A map of the B. juncea genome was constructed using segregation in the F2 population of a combination of restriction fragment length polymorphism (RFLP) and microsatel lite markers. The B. juncea map consisted of 325 loci and was aligned with previous maps of the Brassica A and B genomes. The gene controlling dominant resistance to L. maculans was positioned on linkage group J13 based on segregation for resistance in the F2 population. This position was confirmed in the B1 population in which the resistance gene was definitively mapped in the interval flanked by pN199RV and sB31143F. The provisional location of the recessive gene controlling resistance to L. maculans on linkage group J18 was identified using a subset of informative F2 individuals.Key words: blackleg, B genome, phoma, recessive resistance.

THE POSITION OF LUXOID IN LINKAGE GROUP II OF THE MOUSE

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

motA1552, a mutation of Dictyostelium discoideum having pleiotropic effects on motility and discoidin I regulation.

Genetics ◽  
1988 ◽  
Vol 118 (3) ◽  
pp. 425-436
Author(s):  
S C Kayman ◽  
R Birchman ◽  
M Clarke
Keyword(s):  
Linkage Group ◽  
Dictyostelium Discoideum ◽  
Growth Temperature ◽  
Segregation Analysis ◽  
Pleiotropic Effects ◽  
Temperature Sensitive ◽  
Temperature Induction ◽  
Group Ii ◽  
Unstable Mutations ◽  
Axenic Growth

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.

GENETICS OF SORDARIA FIMICOLA. IX. LINKAGE GROUP II

1975 ◽  
Vol 62 (2) ◽  
pp. 166-171
Author(s):  
Arif S. El-Ani ◽  
L. S. Olive
Keyword(s):  
Linkage Group ◽  
Sordaria Fimicola ◽  
Group Ii

scholarly journals Genetic studies on flagellum mutants of Chlamydomonas reinhardii

1972 ◽  
Vol 19 (2) ◽  
pp. 157-164 ◽  
Author(s):  
Anne McVittie
Keyword(s):  
Linkage Group ◽  
Wild Type ◽  
Linkage Groups ◽  
Genetic Studies ◽  
Chlamydomonas Reinhardii ◽  
The Third ◽  
Group Ii

SUMMARYEight newly isolated 9 + 0 mutants each mapped at one of the four previously known loci. Short flagellum mutants were at three loci, two of which (pf7 and pf8) were closely linked; the third, pf21, was unlinked to these two and mapped on linkage group II. The long flagellum mutants lf1 and lf2 were on linkage groups II and XII respectively. Mutants pf8A and lf1 were both recessive to wild-type. There was no evidence for non-Mendelian flagellum mutants.

Genetics of the tsetse fly Glossina morsitans submorsitans Newstead (Diptera: Glossinidae): further mapping of linkage groups I, II, and III

1999 ◽  
Vol 77 (8) ◽  
pp. 1309-1313 ◽  
Author(s):  
R H Gooding ◽  
C M Challoner
Keyword(s):  
Linkage Group ◽  
X Chromosome ◽  
Aldehyde Oxidase ◽  
Female Offspring ◽  
Tsetse Fly ◽  
Glossina Morsitans ◽  
Group Iii ◽  
Glossina Morsitans Submorsitans ◽  
Group I ◽  
Group Ii

Standard mapping procedures were used to map four loci in linkage group I (the X chromosome), two loci in linkage group II, and two loci in linkage group III of Glossina morsitans submorsitans. In the presence of the allele Srd (the distorter allele favoring production of female offspring), no recombination occurred between any of the following loci: Pgm (phosphoglucomutase), wht (white eye color), Est-X (a thoracic esterase), and Sr (sex-ratio distortion). However, in the absence of Srd (i.e., in females homozygous for Srn, the allele that permits males to sire both female and male offspring in approximately equal numbers), the loci Pgm and wht were separated by 23 ± 4.0% recombination (map distance). These results indicate that ourG. m. submorsitans strains carry two forms of the X chromosome, designated XA and XB. In support of this interpretation, two lines of G. m. submorsitans were established: in both lines, males with wild-type eyes sired families that were almost exclusively female, while males with white eyes sired families having males and females in approximately equal numbers. Two loci, Ao (aldehyde oxidase) and Est-1 (a thoracic esterase) were separated by 6.1 ± 2.3% recombination in linkage group II, and two loci, Mdh (malate dehydrogenase) and Pgi (phosphoglucose isomerase), showed 51.9 ± 4.9% recombination in linkage group III.

scholarly journals The positions of the centromeres in linkage groups II and IX of the mouse

1968 ◽  
Vol 11 (2) ◽  
pp. 193-199 ◽  
Author(s):  
Mary F. Lyon ◽  
Jane M. Butler ◽  
Richard Kemp
Keyword(s):  
Linkage Group ◽  
Close Linkage ◽  
Linkage Groups ◽  
Group Ii ◽  
Significant Linkage

In mice heterozygous for translocation T(2;?)163H, and also for linkage group II markers, the cw locus shows close linkage with the point of rearrangement (about 1−2% recombination). Since T 163 was apparently formed by fusion of two chromosomes near their centromeres, this means that the centromere must lie at the cw end of linkage group II. In homozygotes for T(2; 9)138Ca the genes T and d show significant linkage, indicating that their loci are on opposite sides of the trans-location break. Since, from previous data, the break is known to be proximal to d, it must then be distal to T and, again from previous data, the order of loci hi linkage group IX must be centromere-T-tf-T 138 break.

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