Crest: A Subvital Character in the Budgerigar

[Melopsittacus undulatus]

By: Inte Onsman*, Research coordinator


Research & Advice Group, The Netherlands

* The following article is based on observations made by Ziswiler (1963) [7] and the author himself (1991).

Between 1955 and 1963, 150 testmatings were carried out from which more than 500 youngsters hatched, and only crested budgerigars were used at that time. It is already a well known fact that the crest factor sometimes is lethal and sometimes it is not. To determine the cause of this lethality, fertilized eggs were opened between the 7th and 15th day of incubation and the embryo's were examined. Also on the 19th day of incubation eggs were pealed and the embryo's were measured and fixed.

1) Heterozygous carriers of the crestfactor (Cr/Cr+) are recognized by five different types.
a. Only one single crested feather.
b. Small tuft.
c. Big tuft.
d. Small tuft with saddle manes.
e. Half circular crest.

2) The homozygous carriers (Cr/Cr) are recognized by four different types.
a. Double asymmetry.
b. Frontal tufted and full circular crest on the back of the head.
c. Double full circular crests.
d. Full circular (single) crest.

Further questions were:

1) Is the inheritance autosomal or sex-linked.
2) Is it the pleiotropic effect of a single factor or is it polygenic.
3) Are the different phenotypes of the crest caused by position effect, pseudoallelism or modifying genes.

Testmatings showed that the sex ratio is 1:1, therefore it is not sex-linked but autosomal. These testmatings also showed that this character is not caused by any linkage of genes or by pseudoallelism with position effect. It seems that a single factor with pleiotropic effects is responsible for the crested phenotype. This had also been found in the domestic fowl [3].

Lethality in both heterozygotes and homozygotes is 48%. The crestfactor is a subvital factor showing complete dominance concerning the offspring. Vital carriers of the crestfactor are recognized by tufted feathers on the head.
The development and appearance of the crests is dependent on four different components: abnormal position of the feather follicles on the head, the rapid growth rate of these feathers, the number of featherfollicles involved and, the genetical makeup of the bird. The abnormal position of these feathers depends on a changed polarity and twisted shafts. In some cases even the down feathers show on the outside while the main-feather is completely turned backwards against the body.
Crested feathers usually are longer than normal feathers. In extreme cases crested feathers are even three times longer than normal feathers. Colour and internal structure of crested feathers are equal to normal feathers, only the structure of the barbules is somewhat different. Barbs of crested feathers only have ± 30% normal barbules.
The appearance of the crest is determined by the number of feathers involved. The number of these feathers varies from a single one up to 160. Crests from Cr/Cr and those from Cr/Cr+ birds are well distinguished.
Goessler (1938), showed that the expression of the crest is due to an abnormal involvement of the bone (skull) situated under the skin.

From 30 male budgerigars (Cr/Cr, Cr/Cr+ and Cr+/Cr+), skulls were measured accurately. Out of these 30 skulls, 26 could be divided into two Mendelian classes. The skulls of the Cr/Cr+ class do have an intermediate dimension. The crestfactor does not show complete dominance in these skulls. The skulls of Cr/Cr and Cr/Cr+ birds do not show any difference on their frontside, however the differences on the backside are quite obvious. In general brainsize and skullsize show a certain correlation and therefore it is very interesting to know if there is also such correlation among brainsize and skullsize in crested birds. The hemispheres of the brains of Cr/Cr and Cr/Cr+ birds are significant larger than those from wild-type birds. Brains in heterozygous birds (Cr/Cr+) do have an intermediate size compared to the brains of homozygotes and wild-type birds.
Other parts of the brain, such as the small frontal brains, are not enlarged. Cross-sections of brains showed that the increased size of "crested" brains is based on an abnormal enlargement of the first, second and third ventricle. It has been found that in wild-type birds these ventricles decrease in size during early development and that they remain rather large in crested birds. The enlargement of the lower parts of the ventricles in "crested" brains, suppresses the other parts of the brain.

Behavioral abnormalities
Behavioral abnormalities were seen in 25% of the Cr/Cr+ birds and also in Cr/Cr specimens, the most important are:

a) Muscletrembling; some crested birds are trembling all over.

b) Abnormal position of the head.

c) Disturbed movements such as turning round at the bottom of the cage. Hens suffering from this phenomenon could therefore destroy their own eggs.

d) Coordination disturbances during flying. It was noticed that some birds only could flap about uncoordinately.

e) Abnormal mating behaviour. Homozygous cocks were not able to mate properly and fell convulsing on the ground.

In homozygous crested hens the average egg-size is smaller than in normal hens. The size of an average egg from a normal hen is 19,1 x 15,6mm and, the average egg-size of homozygous (Cr/Cr) crested hens is 16,2 x 14,4mm.

Strongly extended neck muscles at hatching.
Hatching chicks carrying one or two crest factors distinguish themselves from normals by their strikingly bulging neck muscles. The same observations were made by Goessler (1938) on the heads of crested pigeons. This extension is caused by metabolism and disappears three days after hatching.

The lethal crisis.
During genetical analysis it was found that Cr/Cr birds as well as Cr/Cr+ birds suffer from a lethal crisis causing death in 48% of crested embryo's, while the others reach maturity. The effective lethal crisis has been found during the 12th day of incubation. Lethal embryo's are distinguished by an enormous hydrocephalus internus (water on the brain) and die during the 12th day of incubation. The cause of death is internal brain haemorrhages. Already on the 9th day of gestation cross-sections of presumed lethals distinguish themselves from normals. Brain structure in crested birds has obviously been changed and, even certain area's of both hemispheres have fasciated. Compared to normal brains both hemispheres of "crested" brains are extended but do not show any abnormal structure.
A second lethal crisis for the offspring from Cr/Cr hens occurs at hatching because the eggs of such hens are smaller than the eggs of normal hens.

Genetical analysis provide evidence that all discussed phenotypes are caused by pleiotropic effects of a single factor. During the phenocritical phase starting already on the 8th day of incubation, the crest factor develops a certain activity sometimes leading to extended ventricles and sometimes not.

Another complication of the crestsyndrome is the obvious change in dominance during ontogenesis. Because the crest factor is behaving dominant relating to lethality and in Cr/Cr+ birds with respect to Cr/Cr birds, shows no greater viability, the wild-type allele in heterozygous vitals begins to behave as a suppressor. Therefore all cerebral anomalies will develop less strong in Cr/Cr+ birds than in Cr/Cr individuals.

A third noticeable finding is the variable expression of the crest itself. The shape and size varies strongly as has been stated before.


A hereditary factor in the Budgerigar originally found in Canada named crest, is here investigated as to its hereditary-transmission and its pattern of brain damage. The factor "Cr" was shown to be an autosomal subvital factor with a completely dominant lethal effect of 48% penetrance. The lethal effect is monophasic, the effective lethal crisis setting in on the 12th day of incubation. Hetero- and homozygote birds show highly variable expressivities due to a change dominance. The pleiotropic pattern of manifestation of the crest factor results in enlarged cranium, feather crest on head and behavioral anomalies. Viable homozygous hens distinguish themselves from normals by a lesser clutch- and egg-size. The abnormal size of the eggs subject their offspring to a second lethal crisis independent of their own genetical make-up. Characteristics of this hereditary factor, as the high number of break-throughs, the change in dominance and, the variable degree of expressivity of certain phenes, are discussed.

*Lecture held at the International Budgerigar Symposium on the 17th of May 1992.

Consulted and cited Literature:

[1] Bratt J.
    Rare Breed Club, Crested
    F.S.R.B.B.S. Newsletter (december) 1990
[2] Dunn L.C., Jull M.A. (1928)
    On the Inheritance of Some Characters of the Silky Fowl
    Journal of Genetics Vol.19; pp.27-63
[3] Fisher R.A. (1934)
    Crest and Hernia in Fowls Due to a Single Gene Without Dominance
    Science Vol.80; pp.288-289
[4] Goessler E. (1938)
    Untersuchungen ueber die Entwicklung und Entstehung von
    Arch.Julius Klaus Stiftung Vol.13; pp.495-666
[5] Suttle A.D., Sipe G.R. (1932)
    Linkage of Genes for Crest and Frizzle
    Journal of Heredity Vol.23; pp.135-142
[6] Warren D.C., Hutt F.B. (1936)
    Linkage Relations of Crest, Dominant White and Frizzling in the Fowl
    American Naturalist Vol.70; pp.379-394
[7] Ziswiler V. (1963)
    Hereditary Transmission and Manifestation Pattern of the "Haube" Factor,
    a Subvital Factor of the Budgerigar
    Arch.Klaus-Stift.Vererb.Vol.38; pp.145-165

©Inte Onsman
MUTAVI Research & Advice Group

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