of Mice: SM
Inbr (J) 112. White-bellied agouti or black Aw/a
Origin: MacArthur, 1939 by crossing seven stocks including
DBA and selecting for small body size. To Runner 1948, who began b x s
mating. Small body size at birth and weaning, but this relatively small
size tends to disappear as the animals mature. Very low tumour incidence.
Carries a number of relatively rare polymorphic alleles. Maint. by A,J.
Intermediate life-span in conventional conditions (13/22 = 572 days in
males, 14/22 = 591 days in females). Low gross tumour incidence (20/22)
). Life-span, sexes combined, 422
days (Chai, 1959
). High incidence of amyloidosis
(Russell and Meier, 1966
). High porphyrin
content of Harderian gland (4/16) (Margolis, 1971
High spermatazoal beta-glucuronidase activity (2/9) (Erickson,
). Low brain weight in males (15/18) (Storer, 1969). Large brain/body
weight ratio (4/20) (Roderick et al., 1973
1973). Susceptible to skin ulceration by DMBA (cf. 13/22) (Thomas et al., 1973
., 1973). Long survival on Warfarin
(10/12) (Lush and Arnold, 1975
). Low lymphocyte
phytohaemagglutinin response (39/43) (Heiniger
et al., 1975
., 1975). Susceptible to the development of atherosclerosis
on a semi-synthetic high fat diet but in contrast with C57BL/6 and SWR
they had the same level of high-density lipoprotein cholesterol levels
as on chow and high fat diets (3/9) (Nishina
et al, 1993
). A diet containing 15% dairy fat, 1% cholesterol and
0.5% cholic acid did not cause a high incidence of cholesterol gallstones
(like AKR, DBA/2 contrast C57L, SWR, A) (Faulkner
et al, 1995
). Small body weight which differs from that of the large
strain LG/J as a result of about seven quantitative trait loci at one
week and 17 loci at 10 weeks of age. Each locus has a small effect (Cheverud et al, 1996
Inbr ? +16 (H). White-bellied agouti substrain Aw/Aw.
Chai to Bateman (Edinburgh) 1958, to Dickinson 1961, to Lush in early
1970's, to Peters (Harwell), to Nash, to Peters again in 1979. Identical
wth SM/J at seventeen loci, but differs in being Gpi1b
while SM/J is Gpi1a.
This is believed
to be due to residual heterozygosity or mutation rather than genetic contamination
(Peters and Lyon 1986
Chai C. K. (1959) Lifespan
in inbred and hybrid mice. J. Hered. 50, 203-208.
J. M., Routman E. J., Duarte F. A. M., Van Swinderen B., Cothran K., and
Perel C. (1996) Quantitative trait loci for murine growth. Genetics
Erickson R. P.
(1976) Strain variation in spermatazoal -glucuronidase in mice. Genet.
Res. 28, 139-145.
C. B., Davidson M. K., Davis J. K., Schoeb T. R., Simecka J. W., and Lindsey
J. R. (1995) Acute Mycoplasma pulmonis infection associated with coagulopathy
in C3H/HeN mice. Lab. Animal Sci. 45, 368-372.
H. J., Taylor B. A., Hards E. J., and Meier H. (1975) Heritability of
the phytohaemagglutinin responsiveness of lymphocytes and its relationship
to leukemogenesis. Cancer Res. 35, 825-831.
Lush I. E.
and Arnold C. J. (1975) High coumarin 7-hydroxylase activity does not
protect mice against Warfarin. Heredity 35, 279-281.
Margolis F. L.
(1971) Regulation of porphyrin biosynthesis in the Harderian gland of
inbred mouse strains. Arch. Biochem. Biophys. 145, 373-381.
P. M., Wang J., Toyofuku W., Kuypers F. A., Ishida B. Y., and Paigen B.
(1993) Atherosclerosis and plasma and liver lipids in nine inbred strains
of mice. Lipids 28, 599-605.
J. and Lyon M. F. (1986) New substrain of SM, SM/JH. Mouse N.L.
T. H., Wimer R. E., Wimer C. C., and Schwartzkroin P. A. (1973) Genetic
and phenotypic variation in weight of brain and spinal cord between inbred
strains of mice. Brain Res. 64, 345-353.
E. S. and Meier H. (1966) Constitutional diseases, in Biology of the
Laboratory Mouse, 2nd. ed. (Green E. L., ed), pp. 571-587. McGraw-Hill,
Storer J. B. (1966)
Longevity and gross pathology at death in 22 inbred strains of mice. J.
Gerontol. 21, 404-409.
P. E., Hutton J. J., and Taylor B. A. (1973) Genetic relationship between
aryl hydrocarbon hydroxylase inducibility and chemical carcinogen induced
skin ulceration in mice. Genetics 74, 655-659.
INBRED STRAINS OF MICE
Updated 9 Apr. 1998
MRC Toxicology Unit, Hodgkin Building,
University of Leicester,