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Inheritance of broodiness in the domestic fowl M. N. Romanov , R.T. Talbot , P.W. Wilson & P.J. Sharp Published online: 28 Jun 2010.
To cite this article: M. N. Romanov , R.T. Talbot , P.W. Wilson & P.J. Sharp (1999) Inheritance of broodiness in the domestic fowl, British Poultry Science, 40:S1, 20-21, DOI: 10.1080/00071669986611 To link to this article: http://dx.doi.org/10.1080/00071669986611
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GENETICS
Figure. Mean water content of total muscle in 3 strains of chicken. (FB fast-growing broiler, SB slow-growing broiler, L layer).
the potential for growth. However, the curvilinear growth curve of the organ masses, which attain a plateau, indicates that they have reached their asymptotic growth and may be a limiting factor to further growth in the future. The ratio of muscle to internal organ mass is greatest in the FB compared to the SB and the L which is an indication of their larger muscle component. However, although FB have more muscle, it is less mature than the muscle of the SB and the L, which is demonstrated by the
significantly higher hydration of FB muscle (Figure 1). KONARZEWSKI, M., GAVIN , A., WALLIS, I.R. & MCDEVITT, R.M. (1999) Metabolic and organ mass response to selection for high growth rates in the domestic chicken (Gallus domesticus), Physiological and Biochemical Zoology, in press. GYLES, N.R. (1989) Poultry, people and progress. Poultry Science, 68: 1–8. RICKLEFS, R.E. (1985) Modification of growth and development of muscles of poultry. Poultry Science, 64: 1563–1576.
Inheritance of broodiness in the domestic fowl M. N. ROMANOV, R. T. TALBOT, P. W. WILSON AND P. J. SHARP Division of Integrative Biology, Roslin Institute (Edinburgh) EH25 9PS, Scotland Broodiness is a behavioural trait observed in most common breeds of domestic fowl with the exception of the White Leghorn. The genetics of broodiness has been investigated and has produced conflicting observations: some authors have produced evidence suggesting that the trait is polygenic with a major sex-linked effect (review Hutt, 1949; Saeki, 1957; Saeki and Inoue, 1979), while others found no evidence of sex-linked genes for broodiness in the Rhode Island Red (Hays, 1940). The aim of this study was to reassess the possibility that there is a major gene located on the Z chromo-
some implicated in the control of broodiness. The identification of the location of such a gene or its markers would facilitate marker-assisted selection against broodiness. The study involved crossing a White Leghorn male (WL, from an inbred non-broody strain) and Bantam females (B, from a heterogeneous broody strain with a previous history of broodiness), backcrossing an F1 male with WL females, and the production of the reciprocal cross of a B male with WL hens. The female progeny were kept in floor pens with access to nest boxes and hard boiled eggs
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during the course of a photo-induced cycle of egg production. The incidence of broodiness was observed in 2 successive cycles of photo-induced egg laying, except for the backcross progeny, for which only 1st cycle information is currently available. The c 2 test was applied to assess whether or not a difference between a predicted and observed incidence of broodiness was significant. In a preliminary study, 28 B and 28 WL females were tested for broodiness and showed respectively 78·6% and 0% incidence of incubation behaviour. Because the actual penetrance of the trait measured in the B population was 78·6%, this was taken into account when analysing the phenotype segregation in the progeny from the 3 experimental matings. We tested the simplest hypothesis that genetic control of broodiness involves a single dominant broody gene on the Z chromosome (Table). If this hypothesis is correct, there should be no broodiness in the progeny of a WL male and B hens. Contrary to this prediction, it was observed that 45 of 73 (61·6%) F1 females from this cross showed broody behaviour (Table), which was not significantly different from that in the B stock hens (78·6%). In the backcross progeny (F1 male × WL hens), the incidence of broodiness was predicted to be 50%. Again, contrary to this prediction, the incidence of broodiness was very low with only 5 out of 104 showing the trait (4·8%; Table). In the reciprocal mating of a B male with 2 WL females, the incidence of broodiness was predicted to be 100% or at least, the same as that found in the B stock population. Unfortunately, this cross suffered from problems of low fertility in both the males and females, resulting in only 11 female progeny, which is too small a number to allow firm conclusions to be drawn. Six of the 11 hens became broody (54·5%), which was not significantly different from the prediction (Table). Because of the limited data from this mating, the incidence of incubation behaviour in the progeny was also not significantly different from that in the B stock population (78·6%). However, the occurrence of non-broody progeny in this cross is not consistent with the hypothesis of a single dominant sex-linked gene controlling broodiness. Taken together, the observations in this study suggest, as a first approximation, that broodiness is controlled by a dominant autosomal gene at 1 locus in the Bantam and a ‘non-broody’ autosomal gene at another locus in the White Leghorn. Assuming A be an incompletely dominant gene for broodiness and B an incompletely dominant inhibitor of broodiTable. c
2
ness, the parents (P) and progeny (F1) in the test and reciprocal crosses will have the following genotypes: P ?WL × /B P ?B × /WL aaBB AAbb AAbb aaBB F1 ?AaBb; / AaBb F1 ?AaBb; / AaBb Assuming an incomplete dominance of both genes and variable penetrance of the broody trait, we predict an incidence of broodiness of about 50% in female F1 progeny from the test and reciprocal crosses. This is close to the actual values (61·6% and 54·8%, respectively). In the backcross progeny (F2), the segregation will be as follows: P ?F1(?WL × /B) × /WL AaBb aaBB F2 ?1/4AaBB, 1/4AaBb, 1/4aaBB, 1/4aaBb; /1/4AaBB, 1/4AaBb, 1/4aaBB, 1/4aaBb In the backcross progeny, the broody phenotype would be expected in female diheterozygotes (AaBb) which would result in an incidence of broodiness of about 25%. But again, assuming an incomplete dominance of both genes and variable penetrance of the broody trait, only half of them, about 12·5%, would be predicted to become broody. The observed percentage of broodiness was 4·8%, which is significantly less. However, further observations are currently being made during a 2nd cycle of photoinduced egg laying which may uncover further broody phenotypes. These observations are consistent with the view that incubation behaviour in chickens is not controlled by a major gene (or genes) on the Z chromosome. There must therefore be major autosomal genes contributing to the expression of the behaviour. If a broody gene exists on the Z chromosome it is one of at least 3 genes including 2 dominant autosomal ones with probably equal influence. Supported by a BBSRC Core Strategic Grant. M.R. is supported by a Royal Society/NATO Postdoctoral Fellowship while on leave from the Laboratory of Genetics, Poultry Research Institute, Borky, Ukraine. HAYS, F.A. (1940) Inheritance of broodiness in Rhode Island Reds. Massachusetts Agricultural Experiment Station Technical Bulletin, 377. HUTT , F.B. (1949) Genetics of the Fowl (New York, McGraw-Hill). SAEKI, Y. (1957) Inheritance of broodiness in Japanese Nagoya fowl, with special reference to sex-linkage and notice in breeding practice. Poultry Science, 36: 378–383. SAEKI, Y. & INOUE, Y. (1979) Body growth, egg production, broodiness, age at first age and egg size in red jungle fowls, and attempt at their genetic analyses by the reciprocal crossing with White Leghorns. Japanese Poultry Science, 16: 121–125.
test for a major gene controlling broodiness on the Z chromosome in female progeny from crosses between White Leghorns (WL), Bantams (B) and a F1 backcross
Crosses ?WL×/B ?F1(?WL×/B) × /WL ?B×/WL
Obser ved phenotypes
Expected phenotypes
45 broody: 28 non-broody 5 broody: 99 non-broody 6 broody: 5 non-broody
0 broody: 73 non-broody 52 broody: 52 non-broody 11 broody: 0 non-broody
c
2
27´7 85´0 2´3
P
