the menstrual cycle. In the brain the histone code can change in response to addictive drugs such as cocaine, whereas in the cells lining the gut, the pattern of epigenetic modifications will alter depending on the amounts of fatty acids produced by the bacteria in our intestines. These changes in the histone code are one of the key ways in which nurture (the environment) interacts with nature (our genes) to create the complexity of every higher organism on earth.
Histone modifications also allow cells to ‘try out’ particular patterns of gene expression, especially during development. Genes become temporarily inactivated when repressive histone modifications (those which drive gene expression down) are established on the histones near those genes. If there is an advantage to the cell in those genes being switched off, the histone modifications may last long enough to lead to DNA methylation. The histone modifications attract reader proteins that build up complexes of other proteins on the nucleosome. In some cases the complexes may include DNMT3A or DNMT3B, two of the enzymes that deposit methyl groups on CpG DNA motifs. Under these circumstances, the DNMT3A or 3B can ‘reach across’ from the complex on the histone and methylate the adjacent DNA. If enough DNA methylation takes place, expression of the gene will shut down. In extreme circumstances the whole chromosome region may become hyper-compacted and inactivated for multiple cell divisions, or for decades in a non-dividing cell like a neuron.
Why have organisms evolved such complex patterns of histone modifications to regulate gene expression? The systems seem particularly complex when you contrast them with the fairly all-or-nothing effects of DNA methylation. One of the reasons is probably because the complexity allows sophisticated fine-tuning of gene expression. Because of this, cells and organisms can adapt their gene expression appropriately in response to changes in their environment, such as availability of nutrients or exposure to viruses. But as we shall see in the next chapter, this fine-tuning can result in some very strange consequences indeed.
Chapter 5
Why Aren’t Identical
Twins Actually Identical?
There are two things in life for which we are never prepared: twins.
Josh Billings
Identical twins have been a source of fascination in human cultures for millennia, and this fascination continues right into the present day. Just taking Western European literature as one source, we can find the identical twins Menaechmus and Sosicles in a work of Plautus from around 200 B.C.; the re-working of the same story by Shakespeare in The Comedy of Errors , written around 1590; Tweedledum and Tweedledee in Lewis Carroll’s Through the Looking-Glass, and What Alice Found There written in 1871; right up to the Weasley twins in the Harry Potter novels of J. K. Rowling. There is something inherently intriguing about two people who seem exactly the same as one another.
But there is something that interests all of us even more than the extraordinary similarities of identical twins, and that is when we can see their differences. It’s a device that’s been repeatedly used in the arts, from Frederic and Hugo in Jean Anhouil’s Ring around the Moon to Beverley and Elliott Mantle in David Cronenberg’s Dead Ringers . Taking this to its extreme you could even cite Dr Jekyll and his alter ego Mr Hyde, the ultimate ‘evil twin’. The differences between identical twins have certainly captured the imaginations of creative people from all branches of the arts, but they have also completely captivated the world of science.
The scientific term for identical twins is monozygotic (MZ) twins. They were both derived from the same single-cell zygote formed from the fusion of one egg and one sperm. In the case of MZ twins the inner cell mass of the blastocyst split into two during the early cell divisions, like slicing a doughnut in half, and gave rise to two
Histone modifications also allow cells to ‘try out’ particular patterns of gene expression, especially during development. Genes become temporarily inactivated when repressive histone modifications (those which drive gene expression down) are established on the histones near those genes. If there is an advantage to the cell in those genes being switched off, the histone modifications may last long enough to lead to DNA methylation. The histone modifications attract reader proteins that build up complexes of other proteins on the nucleosome. In some cases the complexes may include DNMT3A or DNMT3B, two of the enzymes that deposit methyl groups on CpG DNA motifs. Under these circumstances, the DNMT3A or 3B can ‘reach across’ from the complex on the histone and methylate the adjacent DNA. If enough DNA methylation takes place, expression of the gene will shut down. In extreme circumstances the whole chromosome region may become hyper-compacted and inactivated for multiple cell divisions, or for decades in a non-dividing cell like a neuron.
Why have organisms evolved such complex patterns of histone modifications to regulate gene expression? The systems seem particularly complex when you contrast them with the fairly all-or-nothing effects of DNA methylation. One of the reasons is probably because the complexity allows sophisticated fine-tuning of gene expression. Because of this, cells and organisms can adapt their gene expression appropriately in response to changes in their environment, such as availability of nutrients or exposure to viruses. But as we shall see in the next chapter, this fine-tuning can result in some very strange consequences indeed.
Chapter 5
Why Aren’t Identical
Twins Actually Identical?
There are two things in life for which we are never prepared: twins.
Josh Billings
Identical twins have been a source of fascination in human cultures for millennia, and this fascination continues right into the present day. Just taking Western European literature as one source, we can find the identical twins Menaechmus and Sosicles in a work of Plautus from around 200 B.C.; the re-working of the same story by Shakespeare in The Comedy of Errors , written around 1590; Tweedledum and Tweedledee in Lewis Carroll’s Through the Looking-Glass, and What Alice Found There written in 1871; right up to the Weasley twins in the Harry Potter novels of J. K. Rowling. There is something inherently intriguing about two people who seem exactly the same as one another.
But there is something that interests all of us even more than the extraordinary similarities of identical twins, and that is when we can see their differences. It’s a device that’s been repeatedly used in the arts, from Frederic and Hugo in Jean Anhouil’s Ring around the Moon to Beverley and Elliott Mantle in David Cronenberg’s Dead Ringers . Taking this to its extreme you could even cite Dr Jekyll and his alter ego Mr Hyde, the ultimate ‘evil twin’. The differences between identical twins have certainly captured the imaginations of creative people from all branches of the arts, but they have also completely captivated the world of science.
The scientific term for identical twins is monozygotic (MZ) twins. They were both derived from the same single-cell zygote formed from the fusion of one egg and one sperm. In the case of MZ twins the inner cell mass of the blastocyst split into two during the early cell divisions, like slicing a doughnut in half, and gave rise to two
Similar Books
