• T. C. Carter

      Articles written in Journal of Genetics

    • The position of fidget in linkage group V of the house mouse

      T. C. Carter

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    • Wavy-coated mice: Phenotypic interactions and linkage tests between rex and (a) waved-1, (b) waved-2

      T. C. Carter

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      A hair-waving mutant derived from mice bred by Mr F. W. Coles, and believed to have arisen by spontaneous mutation in 1947, has proved to be indistinguishable from Rex, both phenotypically and genetically. Observations made on heterogeneous material have shown that Rex is not completely dominant, and that there are characteristic phenotypes associated with four other genotypes involving hair-waving mutants, namely,wa-1 wa-1, Re+ wa-1wa-1, wa-2wa-2 andRe+wa-2wa-2; no phenotypic differences were found betweenRe+, Re+ +wa-1 andRe+ +wa-2. The phenotypic differences, which are summarized in Table 4, depend on the shape and amount of ripple in the vibrissae, the appearance of the guard hairs, the grade of waving pattern in the coat and the direction of the sacrolumbar and abdominal and abdominal hair tracts. They vary greatly with age, being most marked at about 13 days, and tend to disappear in the adult. The mutants are to some extent additive andwa-1 has less effect than eitherwa-2 orRe, so thatRe+wa-1wa-1 resemblesRe+ more closely thanReRe, but the reverse is true ofRe+wa-2wa-2; the latter genotype probably impairs viability.

      New segregation data confirm the genetic independence ofRe andwa-1 and lead to a new estimate (42·3±2·9%) of the recombination fraction betweenRe andwa-2 in female gametogenesis.

    • The genetics of luxate mice - I. Morphological abnormalities of heterozygotes and homozygotes

      T. C. Carter

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      Luxate,1x, is a mutant gene in the house mouse which typically tends to cause preaxial polydactyly (including hyperphalangy of the first digit) in the hind feet of heterozygotes and which causes widespread abnormalities of the hind limbs of typical homozygotes, including reduction of the tibia. Homozygotes may also show preaxial polydactyly or oligodactyly, loss of part of the femur and pubis, sacralization of the 26th vertebra and anomalies of the urogenital system, especially hydronephrosis and hydroureter. The forelimbs are unaffected.

      These abnormalities have been studied in a large stock of mice carrying1x, and it was found that the skeletal abnormalities occur primarily in the preaxial elements of the limbs, the few abnormalities of the postaxial elements being secondary. Changes in the soft tissues follow the skeletal changes, muscles generally retaining their expected relationships to the changed skeletal elements, nerves and vessels to the muscles. It was also found that in luxate mice a muscle disappears if its origin is unossified; it inserts on the nearest appropriate part if its normal field of insertion is absent; and a supernumerary unspecialized digit tends to acquire a normal, unspecialized muscle supply. The severity of the renal abnormalities was not necessarily correlated with the severity of the limb abnormalities.

      The mutant is compared with other limb mutants, especially polydactyly in cats (Danforth), diplopodia in poultry (Taylor & Gunns), polydactyly in guinea-pigs (Sewall Wright) and congenital absence of the tibia in mice (Rabaud). It may be a recurrence of the last-named.

    • The genetics of luxate mice - II. Linkage and independence

      T. C. Carter

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      This paper gives new data on the simultaneous segregation of the mutant luxate,lx, in the house mouse, with marker genes at twenty-six other loci. There is no significant evidence of linkage witha, b, bt, c, Ca, d, f, Fu, fz, je, ln, p, pa, Re, ru,Sd, si, U, v, Va, wa-1, wa-2 or sex. Linkage is found betweenlx and the third linkage group mutantWv, with recombination estimated at 17·7±1·2% (standard error); recombination betweenlx and two other markers in this group,hr ands, is estimated at 47·8±3.·7% and 51·2±1·8% respectively. The order of the loci islx, W, hr, s.

    • Stocks for detecting linkage in the mouse, and the theory of their design

      T. C. Carter D. S. Falconer

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      The importance of mapping the chromosomes of the mouse is stressed, and the need for specially designed stocks for routine linkage testing is pointed out.

      The theory of planning linkage tests is outlined, and the new concept of ‘swept radius’ is introduced. This makes it possible (a) to decide, on the basis of efficiency, between a number of alternative procedures that present themselves in the planning of linkage tests; and (b) to design special linkage testing stocks.

      The composition of five specially designed linkage testing stocks is described. By the use of these stocks a gene can be tested against a little over half of the total genetic map, at the cost of raising about 500 test progeny, which is a considerable improvement over what is at present possible.

      An outline is given in Appendix I of the procedure to be adopted for the use of the stocks.

    • A review of independent segregation in the house mouse

      T. C. Carter D. S. Falconer

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      This paper is a review of all published data on the supposed independence of the more important marker genes in the house mouse, using modern statistical methods to combine data from different sources. New data have been added whenever they happened to be available and the published data were lacking or inadequate.

      About three-quarters of the necessary tests of the mutual independence of the known linkage groups (except IV) have been made. The least well-tested genes in the groups arefi, ru, T, v andwa-2

      The evidence suggests that linkage groups, I, II and XI may not be independent, and further investigation is needed.

      We are indebted to Miss Rita Phillips and Mrs Susan Sobey for assistance with some of the classification of mice and abstraction of data in Table 3; to Miss Mary Lyon and Mr G. A. Clayton for new data ons/Va andVa/sex segregations; and to Mr W. S. Russell for assistance with the computing.

    • A mosaic mouse with an anomalous segregation ratio

      T. C. Carter

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      A mouse, heterozygous for the semi-dominant colour and anaemia mutantWv, showed two patches of full pigmentation (i.e. lackingWv); she bred as though her ovaries were partly deficient of the type allele +w. Point mutation and deletion fail to provide satisfactory explanations; non-disjunction provides a possible explanation; somatic reduction and somatic crossing-over, not previously considered as possible mechanisms of mammalian mosaic formation, would fit the facts well. They could also account for some other mosaic mammals which were hitherto difficult to explain. It is established thatWv, like other mutants, is autonomous in its action on pigmentation.

    • Independence of linkage groups i, ii and xi in the house mouse

      T. C. Carter D. S. Falconer

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    • The genetics oe luxate mice - III. horseshoe kidney, hydronephrosis and lumbar reduction

      T. C. Carter

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    • The genetics of luxate mice - IV. Embryology

      T. C. Carter

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      This Paper describes the development of theluxate syndrome in mice. The manifold detects of limbs, urogenital system and lumbar vertebrae are traced back to three underlying causes, namely, (i) a craniad shift of the hind-limb girdle, with (ii) imperfect morphogenetic control, or (iii) loss, of the anterior end of the limb field. Craniad shift of the hind-limb region is demonstrable in 101/2-day embryos. The limb defects give rise to defects of the umbilical arteries; these lead to the urogenital defects. A possible unitary hypothesis is discussed, whereby all the effects of theluxate gene could be attributed to a single gene effect, craniacl shift of the hind-limb inductor relative to a supposedly limited region of limb potency.

    • Genetics of the little and bagg X-rayed mouse stock - With One Text-figure

      T. C. Carter

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      It has long been thought that the bleb-induced developmental defects in the Little & Bagg mouse stock were due to a single main gene, but conflicting views were taken about the inheritance of the many other defects found in the stock. Further genetic investigations were a necessary prelude to developmental studies; they have now been made, using stocks in which the incidence of the rarer defects had been raised by selection. It is concluded that pseudencephaly, acrania, renal agenesis, preaxial Polydactyly and syndactyly of the middle digit are all parts of a syndrome which includes the bleb-induced defects and is due to one main gene; and that hydronephrosis, ectopia viscerum and midcerebral lesions are probably further parts of the same syndrome. The occurrence of each part is conditioned by the genetic background as well as the main gene. Linkage tests with markers in all known linkage groups (except group IV) were negative.

    • Further genetic studies of eleven translocations in the mouse

      T. C. Carter Mary F. Lyon Rita J. S. Phillips

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    • The use of linked masker genes for detecting recessive autosomal lethals in the mouse - With an appendix by J. B. S. Haldane

      T. C. Carter

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      J. B. S. Haldane has recently developed a theory for experiments in which induced autosomal recessive lethals in the monse are detected through their linkage with single marker genes in several different chromosomes. A theory is now given for experiments using several marker genes in one chromosome; linkage group V is taken as an example. It is concluded that the two methods may not differ greatly in their efficiency.

    • A pilot experiment with mice, using Haldane’s method for detecting induced autosomal recessive lethal genes

      T. C. Carter

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      A search has been made for X-ray induced recessive autosomal lethal genes in the mouse, using a method proposed by J.B.S. Haldane; the experiment was intended primarily to test the method. It was found that the method is less efficient for measuring mutation rates than the specific-locus method. Data obtained enabled a lower limit to be set for the X-ray dose required to induce one recessive autosomal lethal in spermatogonia, namely 810r; no upper limit could be set. Relevance to human problems is discussed.

    • Embryology of the Little & Bagg - X-rayed mouse stock

      T. C. Carter

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      The morphology and development of the many defects in mice of the Little & Bagg X-rayed stock have been reinvestigated, in an attempt to resolve the conflicts in the findings of earlier investigators. The observation that blebs occur on pseudencephalic embryos is incompatible with Bonnevie’s hypothesis that they originate as cerebrospinal fluid in the myelencephalon; other observations support Plagens’ hypothesis that the blebs originate as mesenchymal intercellular fluid. No unitary gene action was found. Four pedigrees of causes were constructed covering, respectively, defects of the central nervous system, bleb-induced lesions and defects of the body wall, morphological defects of the hind limbs, and defects of the urogenital system; there were cross-correlations between defects in the first three pedigrees, but the underlying mechanisms were not identified.

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