Genetics of the Fowl: The Classic Guide to Chicken Genetics and Poultry Breeding
By Frederick B. Hutt 1949
Pages 264-265
Recessive Dwarfism, td
It seems probable that the kind of dwarfism for which Landauer (1929) gave a detailed description but no genetic data is the same as that for which Upp (1934) provided extensive genetic data, but less description. The connecting link was provided by Warrens dwarfs, which Landauer found to resemble closely his own specimen and which (according to Warrens data as reported by Upp) segregated from carrier parents in the same ratio as did Upps. Moreover, an earlier brief description of the latters birds by Mayhew and Upp (1932) conforms to that given by Landauer.
Description. These dwarfs show a general retardation of growth which is recognizable at 2 to 4 weeks of age. The outer toe is curled backward, and this is sometimes evident at hatching. The skull is broad and high in relation to its length, and the upper beak is bent downward. The tissues around the eyes appear swollen. The tongue is shortened and swollen. The legs are shortened, more so in the tarso-metatarsus than in the femur and tibio-tarsus. The sacrum is disproportionately small and high, so that the tail seems abnormally high on the body. There is almost no endochondral bone in the shaft of the long bones. Landauer found the thyroids of his specimen to be enlarged and consisting mostly of aplastic tissue with very small cells entirely lacking in colloid. None of the dwarfs became sexually mature.
Upps data indicated that, of 73 dwarfs hatched in one season, half died before reaching 4 weeks of age and the remainder between 4 and 20 weeks. However, Mayhew and Upp earlier reported one bird that lived to be more than a year and a half old. The condition can therefore be considered as an obligate lethat character, with delayed lethal action, or perhaps as a semi-lethal one.
Landauer considered this syndrome as resulting from hypo-function of the thyroid gland and akin to the condition in man designated as myxoedema infantilis. Similarly a brief treatment of one bird with thyroid gland was apparently ineffective in a dwarf 190 days old.
Genetics. Dwarfs of this type are evidently homozygous for a recessive autosomal gene, for which the symbol td (thyrogenous dwarfism) is proposed. In one year Upp (1934) obtained from carrier parents 236 normal chicks and 70 dwarfs, which is a close fit to the expectation of 230:76. Since this observed ratio applied to chicks that hatched and did not include any that died during incubation, it is evident that the lethal action of the mutation is exerted in very few cases during incubation, if at all.
It is noteworthy that the dwarfs of this type studied by Landauer, Warren, and Upp all occurred in Rhode Island Reds, but in three different flocks that were not likely to be closely related.
***********************************************************************
Poultry Breeding and Genetics
R. D. Crawford
Pages 278- 279
Recessive dwarfism (td). This particular type of dwarfism was first reported by Landauer (1929) in a single bird in a Rhode Island Red flock in Maine. The bird was small the the feathers were longer than normal. The thyroid gland was enlarged and consisted of aplastic tissue without colloid. This hypothyroidal condition closely resembled the human condition known as myxoedema infatilis. Although his description of the condition in Rhode Island Reds was extremely detailed, Landauer gave no genetic data.
Upp (1932) and Mayhew and Upp (1932) also reported a hypothyroidal dwarf condition in Rhode Island Reds, the description of which confirmed to that of Landauer (1929). Chicks appeared normal at hatch, but decisive differences began to appear by three weeks of age. Legs were mych shorter in proportion to body size, and the outer toes turned outward and backward. Their heads were wider in the eye region and their beaks were parrot-like. Their tails were carried on a level with the middle of the body with tail feathers directed backward and downward. Chicks were sociable and active, but difficult to raise to maturity. No dwarfs ever became sexually mature. From the pedigree record data, Mayhew and Upp (1932) conclusively showed that this type of dwarfism resulted from homozygosity for a recessive autosomal gene when his results combined with unreported data from Warren gave 428:120 ratio, where a 411:137 ratio would be expected from carrier x carrier matings. Hutt (1949) later proposed the gene symbol td (thyrogenous dwarfism) for this gene.
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Autosomal recessive diseases
In autosomal recessive diseases, both parents must be carriers (i.e., they are clinically normal but have one mutation of a particular gene), and both must pass the mutation to a child in order for that child to be affected. This inheritance pattern is distinctive in that the parents and other relatives of the person with the disease appear to be completely normal, while 25% of their brothers and sisters will share the same disease. This is sometimes called horizontal transmission because there is no expression seen in previous generations by the ancestors and relatives who carry the mutation. Rather, the mutation travels unobserved (silently) within the family and is expressed by siblings in a single generation. Examples of autosomal recessive disease include sickle cell anemia, cystic fibrosis, Tay-Sachs disease, and phenylketonuria.
KEY TERMS
Autosome or autosomal chromosome Chromosomes other than sex chromosomes.
Chromosomes Long strands of DNA complexed with proteins, which contain the genetic information. At the time of conception, an extra, missing, or damaged copy of a chromosome or even a part of a chromosome disrupts normal development.
*When there is interaction between genetic and non-genetic factors, resulting diseases are termed multifac-torial, or polygenic disorders. The inheritance patterns can be quite complex. Most chronic illnesses in humans are multifactorial hereditary disorders. Examples include heart disease, diabetes, stroke, hypertension, cancer, and most forms of mental illness.
*Some inherited diseases are attributed to damaged or improperly distributed chromosomes and are termed chromosomal diseases. Chromosomes are long strands of DNA (deoxyribonucleic acid) complexed with proteins and RNA (ribonucleic acid) that condense and allow for equal distribution of the genes when cells divide. Each chromosome contains hundreds or thousands of genes, and every cell needs to have two copies of each chromosome in order to maintain genetic balance. At the time of conception, an extra copy or missing copy of a chromosome or even a part of a chromosome disrupts normal development. Most chromosomal abnormalities result from simple accidents of chromosome segregation and, as such, they tend not to recur in families. One example of genetic disorder (in humans) that results from chromosomal imbalance is Down syndrome. This condition is caused by the presence of an extra copy of chromosome 21.
Edited to add .....
Here is a photo album of pictures of a couple dwarfs I hatched...
http://s847.photobucket.com/albums/ab31/kathyinmo/12-20-09 Delaware comparison/
For comparison ... a dwarf and a normal sized chick (hatch mates) .....
***********************************************************
These are the 5 dwarf genes I have found when researching.....
dw Recessive. Males are reduced in size by about 43%, females by 26-32%. Multiple alleles have been proposed. dw is responsible for some beneficial effects. dw homozygotes are more resistant to Marek's Disease and spirochetosis, fewer laying accidents, more aggressive immune response. Abnormal eggs are suppressed (soft-shelled, double yolks). Dwarfism, dw, does not effect mortality but does postpone the onset of lay in pullets up to two weeks. Although egg number and mass are slightly decreased by dw, feed efficiency (feed consumption per egg layed) in laying stocks is usually increased 13-25%.
dwB Recessive but shows a dose effect; 'bantam' gene. Females reduced in size by 5-11% and males by about 5% in heterozygotes and 14% in homozygotes. Allelic with dw.
dwM MacDonald dwarf. Reduces body weight by 13.5% and shank length by 9%. Allelic with dw.
Dw+ Wild-type gene. Lack of dwarfing alleles. Allows 'normal' size to develop.
td thyrogenous dwarfism. Autosomal recessive. Lethal or semi-lethal gene. Chicks appeared normal at hatch, but decisive differences began to appear by three weeks of age. Legs were mych shorter in proportion to body size, and the outer toes turned outward and backward. Their heads were wider in the eye region and their beaks were parrot-like. Their tails were carried on a level with the middle of the body with tail feathers directed backward and downward. These dwarfs show a general retardation of growth which is recognizable at 2 to 4 weeks of age. The outer toe is curled backward, and this is sometimes evident at hatching. The skull is broad and high in relation to its length, and the upper beak is bent downward. The tissues around the eyes appear swollen. The tongue is shortened and swollen. The legs are shortened, more so in the tarso-metatarsus than in the femur and tibio-tarsus. The sacrum is disproportionately small and high, so that the tail seems abnormally high on the body. There is almost no endochondral bone in the shaft of the long bones.
----------------------------------------------------------------------------------------------------------------
From: http://www.ajas.info/Editor/manuscript/upload/22-125.pdf
It is known that some genes could reduce the chicken’s
body size. The thyroid dwarfism (td) gene was a
hypothyroidism (Landauer, 1929). The creeper (Cp) gene
was a form of chondrodystrophy caused by an abnormal
cartilage growth (Landauer and Dunn, 1930). Two sexlinked
genes are known to cause dwarfism. A recessive gene
for smaller body size in Bantam breeds (dwB) was found by
Godfrey (1953). The other gene, described by Hutt (1959),
and known as the dwarfism (dw) gene resulted in a
reduction of body weight, representing about 30-40% of the
normal female weight, depending on age and genetic
background, as reviewed by Mérat, 1984.
By Frederick B. Hutt 1949
Pages 264-265
Recessive Dwarfism, td
It seems probable that the kind of dwarfism for which Landauer (1929) gave a detailed description but no genetic data is the same as that for which Upp (1934) provided extensive genetic data, but less description. The connecting link was provided by Warrens dwarfs, which Landauer found to resemble closely his own specimen and which (according to Warrens data as reported by Upp) segregated from carrier parents in the same ratio as did Upps. Moreover, an earlier brief description of the latters birds by Mayhew and Upp (1932) conforms to that given by Landauer.
Description. These dwarfs show a general retardation of growth which is recognizable at 2 to 4 weeks of age. The outer toe is curled backward, and this is sometimes evident at hatching. The skull is broad and high in relation to its length, and the upper beak is bent downward. The tissues around the eyes appear swollen. The tongue is shortened and swollen. The legs are shortened, more so in the tarso-metatarsus than in the femur and tibio-tarsus. The sacrum is disproportionately small and high, so that the tail seems abnormally high on the body. There is almost no endochondral bone in the shaft of the long bones. Landauer found the thyroids of his specimen to be enlarged and consisting mostly of aplastic tissue with very small cells entirely lacking in colloid. None of the dwarfs became sexually mature.
Upps data indicated that, of 73 dwarfs hatched in one season, half died before reaching 4 weeks of age and the remainder between 4 and 20 weeks. However, Mayhew and Upp earlier reported one bird that lived to be more than a year and a half old. The condition can therefore be considered as an obligate lethat character, with delayed lethal action, or perhaps as a semi-lethal one.
Landauer considered this syndrome as resulting from hypo-function of the thyroid gland and akin to the condition in man designated as myxoedema infantilis. Similarly a brief treatment of one bird with thyroid gland was apparently ineffective in a dwarf 190 days old.
Genetics. Dwarfs of this type are evidently homozygous for a recessive autosomal gene, for which the symbol td (thyrogenous dwarfism) is proposed. In one year Upp (1934) obtained from carrier parents 236 normal chicks and 70 dwarfs, which is a close fit to the expectation of 230:76. Since this observed ratio applied to chicks that hatched and did not include any that died during incubation, it is evident that the lethal action of the mutation is exerted in very few cases during incubation, if at all.
It is noteworthy that the dwarfs of this type studied by Landauer, Warren, and Upp all occurred in Rhode Island Reds, but in three different flocks that were not likely to be closely related.
***********************************************************************
Poultry Breeding and Genetics
R. D. Crawford
Pages 278- 279
Recessive dwarfism (td). This particular type of dwarfism was first reported by Landauer (1929) in a single bird in a Rhode Island Red flock in Maine. The bird was small the the feathers were longer than normal. The thyroid gland was enlarged and consisted of aplastic tissue without colloid. This hypothyroidal condition closely resembled the human condition known as myxoedema infatilis. Although his description of the condition in Rhode Island Reds was extremely detailed, Landauer gave no genetic data.
Upp (1932) and Mayhew and Upp (1932) also reported a hypothyroidal dwarf condition in Rhode Island Reds, the description of which confirmed to that of Landauer (1929). Chicks appeared normal at hatch, but decisive differences began to appear by three weeks of age. Legs were mych shorter in proportion to body size, and the outer toes turned outward and backward. Their heads were wider in the eye region and their beaks were parrot-like. Their tails were carried on a level with the middle of the body with tail feathers directed backward and downward. Chicks were sociable and active, but difficult to raise to maturity. No dwarfs ever became sexually mature. From the pedigree record data, Mayhew and Upp (1932) conclusively showed that this type of dwarfism resulted from homozygosity for a recessive autosomal gene when his results combined with unreported data from Warren gave 428:120 ratio, where a 411:137 ratio would be expected from carrier x carrier matings. Hutt (1949) later proposed the gene symbol td (thyrogenous dwarfism) for this gene.
***************************************************************************
Autosomal recessive diseases
In autosomal recessive diseases, both parents must be carriers (i.e., they are clinically normal but have one mutation of a particular gene), and both must pass the mutation to a child in order for that child to be affected. This inheritance pattern is distinctive in that the parents and other relatives of the person with the disease appear to be completely normal, while 25% of their brothers and sisters will share the same disease. This is sometimes called horizontal transmission because there is no expression seen in previous generations by the ancestors and relatives who carry the mutation. Rather, the mutation travels unobserved (silently) within the family and is expressed by siblings in a single generation. Examples of autosomal recessive disease include sickle cell anemia, cystic fibrosis, Tay-Sachs disease, and phenylketonuria.
KEY TERMS
Autosome or autosomal chromosome Chromosomes other than sex chromosomes.
Chromosomes Long strands of DNA complexed with proteins, which contain the genetic information. At the time of conception, an extra, missing, or damaged copy of a chromosome or even a part of a chromosome disrupts normal development.
*When there is interaction between genetic and non-genetic factors, resulting diseases are termed multifac-torial, or polygenic disorders. The inheritance patterns can be quite complex. Most chronic illnesses in humans are multifactorial hereditary disorders. Examples include heart disease, diabetes, stroke, hypertension, cancer, and most forms of mental illness.
*Some inherited diseases are attributed to damaged or improperly distributed chromosomes and are termed chromosomal diseases. Chromosomes are long strands of DNA (deoxyribonucleic acid) complexed with proteins and RNA (ribonucleic acid) that condense and allow for equal distribution of the genes when cells divide. Each chromosome contains hundreds or thousands of genes, and every cell needs to have two copies of each chromosome in order to maintain genetic balance. At the time of conception, an extra copy or missing copy of a chromosome or even a part of a chromosome disrupts normal development. Most chromosomal abnormalities result from simple accidents of chromosome segregation and, as such, they tend not to recur in families. One example of genetic disorder (in humans) that results from chromosomal imbalance is Down syndrome. This condition is caused by the presence of an extra copy of chromosome 21.
Edited to add .....
Here is a photo album of pictures of a couple dwarfs I hatched...
http://s847.photobucket.com/albums/ab31/kathyinmo/12-20-09 Delaware comparison/
For comparison ... a dwarf and a normal sized chick (hatch mates) .....
***********************************************************
These are the 5 dwarf genes I have found when researching.....
dw Recessive. Males are reduced in size by about 43%, females by 26-32%. Multiple alleles have been proposed. dw is responsible for some beneficial effects. dw homozygotes are more resistant to Marek's Disease and spirochetosis, fewer laying accidents, more aggressive immune response. Abnormal eggs are suppressed (soft-shelled, double yolks). Dwarfism, dw, does not effect mortality but does postpone the onset of lay in pullets up to two weeks. Although egg number and mass are slightly decreased by dw, feed efficiency (feed consumption per egg layed) in laying stocks is usually increased 13-25%.
dwB Recessive but shows a dose effect; 'bantam' gene. Females reduced in size by 5-11% and males by about 5% in heterozygotes and 14% in homozygotes. Allelic with dw.
dwM MacDonald dwarf. Reduces body weight by 13.5% and shank length by 9%. Allelic with dw.
Dw+ Wild-type gene. Lack of dwarfing alleles. Allows 'normal' size to develop.
td thyrogenous dwarfism. Autosomal recessive. Lethal or semi-lethal gene. Chicks appeared normal at hatch, but decisive differences began to appear by three weeks of age. Legs were mych shorter in proportion to body size, and the outer toes turned outward and backward. Their heads were wider in the eye region and their beaks were parrot-like. Their tails were carried on a level with the middle of the body with tail feathers directed backward and downward. These dwarfs show a general retardation of growth which is recognizable at 2 to 4 weeks of age. The outer toe is curled backward, and this is sometimes evident at hatching. The skull is broad and high in relation to its length, and the upper beak is bent downward. The tissues around the eyes appear swollen. The tongue is shortened and swollen. The legs are shortened, more so in the tarso-metatarsus than in the femur and tibio-tarsus. The sacrum is disproportionately small and high, so that the tail seems abnormally high on the body. There is almost no endochondral bone in the shaft of the long bones.
----------------------------------------------------------------------------------------------------------------
From: http://www.ajas.info/Editor/manuscript/upload/22-125.pdf
It is known that some genes could reduce the chicken’s
body size. The thyroid dwarfism (td) gene was a
hypothyroidism (Landauer, 1929). The creeper (Cp) gene
was a form of chondrodystrophy caused by an abnormal
cartilage growth (Landauer and Dunn, 1930). Two sexlinked
genes are known to cause dwarfism. A recessive gene
for smaller body size in Bantam breeds (dwB) was found by
Godfrey (1953). The other gene, described by Hutt (1959),
and known as the dwarfism (dw) gene resulted in a
reduction of body weight, representing about 30-40% of the
normal female weight, depending on age and genetic
background, as reviewed by Mérat, 1984.
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