Cattle

DNA technologies have revolutionised modern science in many ways. DNA (Deoxyribonucleic acid), the hereditary material in all living organism from bacteria to animals and humans, controls and directs all the functions of a living organism. Many techniques have been developed to understand and manipulate DNA for purposes like parentage analysis, curing genetic diseases, forensics, gene therapy and to improve livestock production.

Various different DNA based technologies are available for application in the production enterprises. With many more under development, it makes sense to be informed about the basic theory of DNA and the current applications available before making the decision to invest in DNA technologies.

Animal Genetics price list documents can here found here.

  • Cattle – 3-in-1 (DNA / Pompe’s / CMS)

    Pompe’s disease is a glycogen storage disorder confined to grey Brahman cattle.  The conversion of glycogen to glucose is catalyses by the enzyme acid alpha-glycosidase.  A defect in the function of this enzyme causes a build-up of glycogen leading to muscle weakness throughout the body including the heart.

    Congenital Myasthenia Syndrome (CMS) is an auto-immune disorder found mainly in red Brahman cattle and is characterized by varying degrees of progressive general muscle weakness. This weakness is caused by defective nerve-muscle interaction. Affected animals have to be hand fed.

    Both, Pompe’s syndrome and CMS are autosomal recessively inherited genetic disorders where carriers of the disorders cannot be phenotypically distinguished. The average life expecting of a Pompes and CMS affected calves is less than 12 months and should be culled.

    Carriers of recessive disorders perform normally.  Crossing two carriers results in a 25% chance for an affected progeny.  It is therefore important to know the status of all animals to be used for breeding purposes in a stud.  This information can then be used when making mating decisions.

    Autosomal recessive inheritance is characterized by the following:

    • The defective gene must be transmitted from BOTH parents to produce an affected offspring.
    • Both parents must be carriers (heterozygous) for the disorder to produce an affected offspring.
    • When two carriers are mated they can breed progeny that are either affected (homozygotes) or carriers (heterozygotes) or normal (no mutant gene).
    • If the offspring of a cross between two carriers is proven to be normal (no defective gene) the possibility of the disorder manifesting ends in this progeny

    Crosses may be illustrated as follows:

    Purely from a scientific point of view advice would be the following:

    Do line breeding and crossing with animals that are non-carriers of Pompe’s Syndrome and CMS, or cross a carrier animal with a non-carrier. If crossings are allowed between carriers and non-carriers confirm the status of the offspring for future breeding purposes.

  • Curly Calf Syndrome

    Curly calf syndrome is a lethal genetic defect that has been identified in beef cattle. Calves are stillborn and have a twisted or curved spine and extended and contracted limbs, hence the term “curly calf syndrome.” This is a lethal genetic defect scientifically known as Arthrogryposis Multiplex (AM) The tern AM is a Greek derivation which means curved or hooked joints. This congenital defect was discovered in the Angus breed and genetically traced to a popular certain bull (GAR Precision 1680) in that breed. The mode of inheritance for this condition is a simple recessive gene. This is a pattern of inheritance is similar to coat colour for black and red in cattle or horned or polled. Animals with only one copy of the AM gene and one copy of the normal gene appear normal and are known as carriers. Carrier animals are normal, perform as good as non-carriers, but when mated to a carrier female can there is a 25% chance for the offspring to be affected. 50% of the offspring can be carriers for AM while there is a 25% chance for “clean” offspring. The condition (curly calf syndrome) can only be expressed when the individual is homozygous for the AM gene ( both genes are present in the affected calf) for the trait.

    A DNA based test has been developed to identify individuals that have one copy or no copies of the AM gene. Animals testing free of the AM gene are designated as AMF (AM Free). Not all animals need to be tested, only those that have ancestors in their pedigree that are known carriers would be necessary to eliminate the chance of the occurrence of curly calves in a breeding program.

  • Cytogenetics: 1/29 Translocation

    The genetic blueprint of any organism is reflected in DNA genome. During cell dividion the DNA strands are folded round proteins and histones forming cellular structures called chromosomes of which each living organism has a unique number.  These chromosomes consist of two haploid sets (single set) of chromosomes, one inherited from the mother and one from the father.

    These haploid sets of chromosomes are found in the germ-cells (sperm and ova) and when fertilised ovum is formed with a diploid set of chromosomes (two sets).

    In the case of cattle the diploid number of chromosomes is 60, with cows having two X-chromosomes and bulls having one X- and one Y-chromosome.  By viewing a karyotype of an animal a picture of the chromosomes is obtained and any apparent chromosomes may be identified.  A translocation occurs when two chromosomes fuse to form one single chromosome.  In the case of cattle such animals will have 59 chromosomes and not 60.  As no genetic material is lost during such a fusion, carriers of such a translocation are completely normal and can achieve similar standards to normal non-carrier cattle.

    The most common and well documented known translocation in cattle is the translocation between chromosome 1 and 29, also known as the 1/29 translocation.  This translocation has been documented in several breeds of cattle including:  Limousine, Blonde D’Aquitan, Charolais, Ramagnola, Norwegian Red and White, Simmentaller and Brown Swiss.

    Based on the principle of independent segregation a carrier of the translocation has a 50% chance of transmitting the translocation to offspring.  At the same time there is a 50% chance that the offspring will not have the translocation and when crossed with other non-carriers of the translocation this genetic entity is eliminated out of the particular bloodline.

    Theoretically, however, carriers of the 1/29 translocation will have a lower calving percentage compared to non-carrier stock.  The cause can be illustrated as follows:

    (Illustrations by: Department of Animal and Poultry Science, University of Saskatchewan, Saskatoon, Canada S7N 5A8)

    50% of the possible gametes formed during fertilisation will have an unbalance genetic material content and will not develop after fertilisation.  This usually results in a very early miscarriage and cows will usually come on heat within three to four weeks again.

    It should be stressed that, although the 1/29 translocation causes a slightly lower calving percentage, animals carrying the translocation are completely normal and do not influence stock quality, growth or development.  Should siblings carry a translocation, consideration may be given to commercialising the siblings instead of use as registered stock.

  • DNA Profile / Parentage

    It is the goal of all cattle breeders to make genetic progress within their own herds and ultimately take their choice of cattle breed foreword as a whole. Phenotypic selection and performance data have contributed immensely to making wise selection decisions to improve the quality of stock by measuring and recording. There are underlying genetic differences among individuals in a population and it is these underlying genetic differences that influence the phenotypes (performance). However, great technology strides have also been made in the last 15 years and DNA testing is central to ongoing genetic progress and genomic information. Ultimately genetically improved performance data (genomic EBVs) will provide added impedance to early accurate selection decisions and matings.

    Both Bull 1 and Bull 2 match as sire

     

    Bull 2 is excluded as sire

                       
    DNA Marker Calf   Bull 1   Bull 2 DNA Marker Calf Dam Bull 1   Bull 2
    TGLA227 77 101   77 77   87 101 TGLA227 77 101 93 101 77 77   87 101
    BM2113 127 133   133 139   127 133 BM2113 127 133 127 139 133 139   127 133
    TGLA53 166 184   154 184   166 166 TGLA53 166 184 160 166 154 184   166 166
    ETH10 221 221   211 221   119 221 ETH10 221 221 211 221 211 221   119 221
    SPS115 248 254   248 254   248 248 SPS115 248 254 248 248 248 254   248 248
    TGLA126 115 123   117 123   123 123 TGLA126 115 123 115 117 117 123   123 123
    TGLA122 137 149   137 149   137 149 TGLA122 137 149 137 143 137 149   137 149
    INRA23 202 214   208 214   202 208 INRA23 202 214 196 202 208 214   202 208
    ETH3 127 127   117 127   115 127 ETH3 127 127 121 127 117 127   115 127
    ETH225 150 160   148 150   160 160 ETH225 150 160 148 160 148 150   160 160
    BM1824 180 192   192 192   180 188 BM1824 180 192 178 180 192 192   180 188
    CSRM60 92 110   100 110   92 112 CSRM60 92 110 92 100 100 110   92 112
    CSSM66 189 189   189 197   189 197 CSSM66 189 189 189 189 189 197   189 197
    BM1818 262 262   260 262   260 262 BM1818 262 262 262 270 260 262   260 262
    ILSTS006 288 292   292 292   288 290 ILSTS006 288 292 288 294 292 292   288 290
                       

    Both Bull 1 and Bull 2 match as sire if the dam is not tested

     

    Bull 2 is excluded as sire on 7 DNA markers if the dam is included in the test

    The example illustrates the use of the ISAG approved 15 DNA markers. This marker panel has been statistically validated and provides a very high level of accuracy. Accuracy is measured as “the ability of the panel to exclude an incorrect parent from a calf’s pedigree”. For all breeds, 99.99% of incorrect matings will be detected by parentage analysis. In cases where one parent (the sire) is considered, this figure is reduced to around 98% to 96% depending on the breed. In cases where closely related sires are run together in cow herds, ambiguous results may also be obtained if dams are not included. Incorrect paternity may be reported.The point of entry for genetic improvement is always a correct and accurate pedigree (family tree). As the performance of a proven bull is measured through the performance of his progeny, accurate pedigree recording is key to increasing genetic gain. An accurate pedigree allows accurate evaluation of animal performance which is essential when estimated breeding values (EBVs) are being used as the basis for selection.  Parentage testing is a powerful tool for cattle producers to increase the rate of genetic gain in their herds. Contrary to the practice to only determine the sire for breeding confirmation, it is advisable to verify breeding using both the sire and dam. The practice to do line breeding and some inbreeding, narrows the gene pool and only confirming the sire may lead to ambiguous results. In closely related crosses more than one sire may match the calf and the dam must be tested to identify the correct sire and confirm parentage. The illustration is a classic example of this.

    Advantages of DNA-Based Parentage Testing.

    • DNA profiles provide the only “tamper proof” tool to ensure correct individual identification of animals ensuring a unique, permanent DNA ID for tractability
    • Proof of parentage makes it possible to determine which bull sires quality progeny
    • A bull’s service capacity can be determined.
    • Contributes in identifying differences in genetic potential of calves
    • Assists to terminate feeding bulls that are not contributing to the next generations
    • Provides essential evidence for stock theft cases.
    • Increases reliability and accuracy of EBV’s
    • DNA certified pedigrees to comply with breed association requirements
    • Quality control for AI, ET and multiple-sire calves
    • Allows accurate population and family studies
    • Samples can be archived for future testing
  • Genomic SNP Chips

    Unistel offers genomic testing in close co-operation with Neogen Geneseek for customised 50K chips and high density 150K chips for both beef and dairy cattle. The information provided can be utilized directly in the generation of genomic enhanced breeding values or stored for future use. Igenity genetic profiles are extracted from the SNP data and supplied to clients as a handy “add-on”. This information has added a handy “tool” to selection and mating processes.

    The following information can be obtained from the Igenity genetic profiles:

     

    Beef:
    • Residual feed intake
    • Average daily gain
    • Tenderness
    • Marbling
    • Quality grade
    • Yield grade
    • Fat thickness
    • Ribeye area
    • Heifer pregnancy rate
    • Stayability
    • Calving ease
    • Docility
    • Myostatin
    • Coat color (homozygous black)
    • Breed specific horned/polled
    • Multisire parentage
    • Bovine viral diarrhea – persistent infection (BVD-PI) diagnostic test
    • Multiple breed-specific genetic defect tests

    Dairy:

    Health Traits Type Traits
    • Net merit
    • Daughter
    • Pregnancy rate
    • Productive life (months)
    • Somatic cell score
    • Final score (PTAT)
    • Feet/legs
    • Composite
    • Udder composite
    • Stature
    • Strength
    • Body depth
    • Dairy form
    • Rump angle
    • Thurl width
    • Rear legs side view
    • Rear legs rear view
    • Foot angle
    • Feet and leg score
    • Fore attachment
    • Rear udder height
    • Udder cleft
    • Udder depth
    • Front teat placement
    • Rear teat placement
    • Teat length
    • Total Performance Index® (TPI)**
    Yield Traits
    • Milk
    • Fat (lbs)
    • Fat (%)
    • Protein (lbs)
    • Protein (%)
    Calving Traits
    • Daughter calving
    • Ease
    • Daughter stillbirth
  • Myostatin

    Definition:
    Double muscling or muscular hypertrophy is an inherited condition in cattle, characterised by hyperplasia (increase in number) and, to a lesser extent, hypertrophy (enlargement) of muscle fibres.

    Characteristics of the Double Muscling Syndrome:
    Muscle:
    Double-muscled animals are characterized by an increase in muscle mass of about 20%, due to general skeletal muscle hyperplasia and, to a lesser extent, hypertrophy.
    This relative increase in the number of muscle fibres (hyperplasia) occurs during intra-uterine development, such that double-muscled cattle possess nearly twice the number of muscle fibres at birth as do normal cattle.  The muscles of double-muscled cattle also have a significantly reduced amount of connective tissue (collagen).  Not only is collagen reduced in amount, but it is structurally different to normal collagen in that it has a lower proportion of stable, non-reducible, cross-links.  Muscular hypertrophy and hyperplasia is not uniform throughout the beast, being minimal around the neck and increasing as one moves to the hindquarters where it is maximal. This distribution results in the caecases of double-muscled animals having a higher proportion of “expensive” cuts of meat relative to carcases of normal cattle.

    Bone:
    The bone mass of double-muscled cattle tends to be around 10% less than that of normal cattle. This is primarily due to their long bones being shorter, more slender, and of lower density.
    This reduced bone mass results in a significantly higher muscle : bone ratio in double-muscled cattle.

    Fat:
    Double-muscled cattle exhibit hypodevelopment of their fatty tissues. This is due to a reduction in the volume of fat cells rather than to a reduction in their numbers.  Not only is the total fat content reduced, but its composition is different, with double-muscled animals having a much higher percentage of polyunsaturated fats (11% compared with 5% in normal cattle).

    Physiology:
    During forced exercise, double-muscled cattle show signs of fatigue faster than normal cattle. This is thought to be due to a reduced capacity for aerobic metabolic activity by the exercising muscles.  Double-muscled cattle tend to have a reduced tolerance for heat stress. This is thought to be due to the increased heat production associated with their increased muscle mass.

    Reproduction and Growth:
    The syndrome of double muscling is associated with a number of reproductive problems. In the case of those animals where the syndrome is fully expressed there may be:

    1. delays in puberty.
    2. reduced fertility due to an increased incidence of mortality in double-muscled embryos,
    3. increased incidence of dystocia,
    4. reduced milk production,
    5. increased calf mortality.

    Most double-muscled calves tend to have higher birth weights and higher pre-weaning growth rates than their normal contemporaries. Post-weaning, however, their growth rate tends to fall behind that of their normal contemporaries; this appears to be due to a lower feed intake.  If muscle weight gain per unit energy intake is taken into account, double-muscled cattle have better feed efficiency than normal cattle.

    Carcase:
    When compared with normals, the carcases of double-muscled cattle have many desirable characteristics:

    Higher dressing percentage:
    The carcases of double-muscled cattle dress out at between 65 and 70 percent. This is due to a combination of:

    1. increased muscle mass,
    2. reduced body fat,
    3. reduced bone mass, and
    4. smaller internal organs.

    Higher proportion of “expensive” cuts of meat:
    This is due to the non-uniform distribution of the muscular hypertrophy and hyperplasia which is found in double-muscled cattle.  Reduced fat content with a higher proportion of polyunsaturated fats:
    (See above)

    Better meat quality:
    Meat from double-muscled cattle is significantly more tender than that from normal cattle. Much of this is thought to be due to its lower collagen content and to the fact that what collagen is present is not as tough due to its lower proportion of stable, non-reducible, cross-links.

    The significance for producers is that double-muscled animals produce a higher proportion of desirable cuts of lean meat with greater efficiency than do comparable, conventional cattle. For consumers, this meat is more tender and, being lean and having a higher polyunsaturated fat content, conforms more closely with current nutritional guidelines than meat from normal animals.

  • Wagyu Cattle Testing for Claudin 16 Type 1 and Type 2

    Claudin-16 is a genetic disorder that can result in diarrhoea, retarded growth, overgrown hooves as well as terminal kidney failure (terminal interstitial nephritis with excess fibrous connective tissue or zonal fibrosis) in Wagyu cattle. The disorder can present itself at any time from late adolescence and cattle diagnosed with Claudin-16 are unlikely to live longer than 6 years. Heterozygous cattle (carriers of the mutant allele) are not affected and can phenotypically be similar to homozygous normal cattle. However, they may transmit this disease to their offspring. Unistel Animal Services (UAS) offers a test to determine whether cattle have mutated copies for either Type 1 or Type 2 Claudin-16.

  • Wagyu Cattle Testing for Chediak-Higashi Syndrome

    Chediak-Higashi Syndrome (CHS) is a genetic disorder in Wagyu cattle that affects the immune system, as well as other parts of the body. It characterised by a weakened immune system, oculocutaneous albinism (abnormally light pigmentation of the skin, hair, and eyes), blood clotting problems, and nervous system abnormalities resulting in weakness, difficulty walking, and seizures. As complications from this syndrome can become life-threatening, it is essential that carrier individuals not be bred with one another, so as to avoid producing affected offspring. Heterozygous cattle (carriers of the mutant allele) are not affected and can phenotypically be similar to homozygous normal cattle. However, they may transmit this disease to their offspring. Unistel Animal Services (UAS) offers a test to determine whether cattle have mutated copies of the CHS1 gene which could result in Chediak-Higashi Syndrome.