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Monozygotic twins or Identical twins occur when a single egg is fertilized to form one zygote (monozygotic) which then divides into two separate embryos. The two embryos develop into fetuses sharing the same womb. When one egg is fertilized by one sperm cell, and then divides and separates, two identical cells will result. Depending on the stage at which the zygote divides, identical twins may share the same amnion (in which case they are known as monoamniotic) or not (diamniotic). Diamniotic identical twins may share the same placenta (known as monochorionic) or not (dichorionic). All monoamniotic twins are monochorionic. Also note that any monochorionic or monoamniotic twins are identical twins. This condition does not occur in fraternal twins.
The later in pregnancy that twinning occurs, the more structures will be shared. Zygotes that twin at the earliest stages will be diamniotic and dichorionic ("di-di"). Twinning between 4 to 8 days after fertilization typically results in monochorionic-diamniotic ("mono-di") twins. Twinning between 8 to 12 days after fertilization will usually result in monochorionic-monoamniotic ("mono-mono") twins. Twinning after 12 days post-fertilization will typically result in conjoined twins.
In placental species, twins sharing the same amnion (or the same amnion and placenta/chorion) can cause complications in pregnancy. For example, the umbilical cords of monoamniotic twins can become entangled, reducing or interrupting the blood supply to the developing fetus. About 50% of mono-mono twins die from umbilical cord entanglement. Monochorionic twins, sharing one placenta, usually also share the placental blood supply. These twins may develop such that blood passes disproportionately from one twin to the other through connecting blood vessels within their shared placenta, leading to twin-to-twin transfusion syndrome.
Monozygotic twins are genetically identical (unless there has been a mutation in development) and they are the same gender. (On extremely rare occasions, an original XXY zygote may form monozygotic boy/girl twins by dropping the Y chromosome for one twin and the extra X chromosome for the other.) Monozygotic twins generally look alike. Fine physical details such as fingerprints will differ. As they mature, identical twins often become less alike because of lifestyle choices or external influences.
The likelihood of a single fertilisation resulting in identical twins is a random event, not a hereditary trait, and is uniformly distributed in all populations around the world. This is in marked contrast to fraternal twinning which ranges from 1 or 2 per thousand births in Japan (similar to the rate of identical twins) to 14 and more per thousand in some African states The exact cause for the splitting of a zygote or embryo is unknown.
Studies have shown that identical twins reared in different environments share similar personality traits, mannerisms, job choices, attitudes, and interests. These findings add to the belief that many of our behaviors are derived from our genes.
Identical twins have identical DNA but differing environmental influences throughout their lives affect which genes are switched on or off. This is called epigenetic modification. A study of 80 pairs of human twins ranging in age from 3 to 74 showed that the youngest twins have relatively few epigenetic differences. The number of differences between identical twins increases with age. 50-year-old twins had over three times the epigenetic difference of 3-year-old twins. Twins who had spent their lives apart (such as those adopted by two different sets of parents at birth) had the greatest difference. (Fraga, et al., 2005).
To determine whether a disease is caused by genetic factors, researchers study the pattern inheritance of the disease in families. This provides qualitative information about the disease (how it is inherited). A classic example of this method of research is inheritance of hemophilia in the British Royal Family. More recently this research has been used to identify the Apoliprotein E (ApoE) gene as a susceptibility gene for Alzheimer's Disease, though some forms of this gene - ApoE2 - are associated with a lower susceptibility. To determine to what extent a disease is caused by genetic factors (quantitative information), twin studies are used. Monozygotic twins are genetically identical and likely share a similar environment whereas dizygotic twins are genetically similar and likely share a similar environment. Thus by comparing the incidence of disease (termed concordance rate) in monozygotic twins with the incidence of disease in dizygotic twins, the extent to which genes contribute to disease can be determined. Candidate disease genes can be identified using a number of methods. One is to look for mutants of a model organism (e.g. the organisms Mus musculus,Drosophila melanogaster, Caenhorhabditis elegans,Brachydanio rerio and Xenopus tropicalis) that have a similar phenotype to the disease being studied. Another approach is to look for segregation of genes or genetic markers (e.g. single nucleotide polymorphism or expressed sequence tag) (Fig. 2).
A large number of SNPs spaced throughout the genome have been identified recently in a large project called the HapMap project). The usefulness of the HapMap project and SNP typing and their relevance to society was covered in the 27th October 2005 issue of the leading international science journal Nature (Fig 3).
A large number of genes have been identified that contribute to human disease. These are avaialble from the US National Library of Medicine, which has an impressive range of biological science resources available for free online. Amongst these resources is Online Mendelian Inheritance in Man - OMIM that provides a very, very comprehensive list of all known human gene mutations associated with, and likely contributing to, disease. Each article at OMIM is regularly updated to include the latest scientific research. Additionally, each article provides a detailed history of the research on a given disease gene, with links to the research articles. This resource is highly valuable and is used by the world's top science researchers.
References & Bibliography
- McVean G, Spencer CC, Chaix R (2005). Perspectives on human genetic variation from the hapmap project. PLoS Genet 1 (4): e54.This review is free of charge
- Skelding K.A., Gerhard GS, Simari RD, Holmes DR Jr (2007). The effect of HapMap on cardiovascular research and clinical practice. Nat Clin Pract Cardiovasc Med 4 (3): 136-142.