By F. G. Biddle, F. C. Fraser (auth.), James G. Wilson, F. Clarke Fraser (eds.)
Modification of embryonic improvement via genetic ameliorations within the mom is a well-regcognized phemomenon, yet little is understood concerning the genet ics of those maternal qualities or the mechanisms wherein they act. to demonstrate the genetic method of the matter, examples are given of ways changes in embryonic reaction to a teratogen may be partitioned into these caused by ameliorations in embryonic genotype (including the potential position of X-linked genes in generating reciprocal pass differences), maternal genotype, and cytoplasmically transmitted elements. the benefits and barriers of research via acceptable crosses, in utero remedies, embryo transfers, and in vitro experiments are illustrated. the various inbred lines of the mouse, with well-documented body structure, the lately built recombinant inbred lines, and the life of simply pointed out biochemical marker genes provide at tractive possibilities, to date mostly unexploited, for causal research of mater nal results on teratological responses. VII. ADDENDUM for the reason that this bankruptcy used to be written, a number of proper papers have seemed. the tension distinction among AI] and C57BU6] mice in frequency of cleft-palate reaction to cortisone was once suited to a version of in general dispensed log tolerance (Biddle and Fraser, 1976). Genetic variations, either in maternal uterine surroundings and embryonic reaction, may be represented when it comes to their influence at the median potent dose required for the cleft-palate re sponse. The maternal impact of AI] dams relative to C57BU6] dams brought on a two-fold relief in embryonic tolerance to cortisone-induced cleft palate.
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Additional info for Comparative, Maternal, and Epidemiologic Aspects
1974, Hairpin-tail: A case of post-reductional gene action in the mouse egg? Genetics 76:795. , and Wallace, M. , 1973, Histidinaemic mutant in the mouse, Nature (Londcm) 244:77. , Mya, K. , Wright, A. , and Lyon, M. , 1977, Maternal histidine metabolism and its effect on foetal development in the mouse, Nature 265:262. , 1954, The inheritance of susceptibility to the teratogenic action of cortisone in mice, Genetics 39: 185. , 1965, Interplay of intrinsic and extrinsic factors, in: Teratology; Principles and Techniques O.
And Son, C. D. 1968, Maternal phenylketonuria: Implications for growth and development,]. Pediatr. 73:560. Fraser, F. , and Fainstat, T. , 1951, Production of congenital defects in the offspring of pregnant mice treated with cortisone, Pediatrics 8:527. Fraser, F. , Walker, B. , and Fainstat, T. , 1954, Experimental production of deft palate with cortisone and other hormones,]. Cell Compo Physiol. ):237. Fuller, R. , and Shu~n, J. , 1974, Genetic divergence in relatives of PKU's: Low IQ correlation among normal siblings, Dev.
LN~ I yH2 ryH2H2 /N, /N" CH 3 CH3 2·HYDROXY· IMIPRAMINE CH # N ~OH I 2 CH2 CD) H H DESDIMETHYL IMIPRAMINE ! (0)" I ~H2 ~H2 DESIPRAMINE ~ I .. NI /N" CH3 H IMIPRAMINE CH "'" rH2 r H2 /N" CH 3 CH 3 ...... J H-y 2·HYDROXY ·IMIPRAMINE GLUCURONIDE 0 COOH CH3 H 2·HYDROXYDESMETHYL· IMIPRAMINE ~ a:DS~I I -UH I CH HO-C-H I 2 CH I 2 CH2 N I H- y COOH /'\. CH3 H 2·HYDROXYDESMETHYL·IMIPRAMINE GLUCURONIDE Fig. 4. Pathways of imipramine metabolism. , 1975). , 1967). Some substances, such as hexobarbital, aminopyrine, and ethylmorphine, cause a decrease in the spectrum at about 417 nm and an increase at about 391 nm; such substances are called type-I compounds.