Evolution of a Fruit Fly, Evolution of a Human
22/09/10 18:19 Filed in: GenomeWeb Daily Scan
Submitted by S. Pelech - Kinexus on Wed, 09/22/2010 - 18:19.
At 25°C, the average Drosophila melanogaster can bred after about 8.5 days after birth, and in its life span of around 30 days lays about 400 eggs, usually 5 at a time. Human females are capable of reproduction usually from 12 years of age. However, historically in human societies, the average generation time appears to be about 20 years.
In the UC Irvine study by Burke et al., the genomes of the flies were analyzed after 600 generations with selective pressure for accelerated development. This would extrapolate to approximately 12,000 years in humans. As most researchers would have predicted, the increased rate of sexual development in the flies by selective breeding was due to the acquisition of mutations in many genes. Indeed, this supports the idea that "soft sweeps" underlie complex traits. However, it is also well appreciated that occasionally mutations can arise in genes that encode key regulatory proteins such as kinases and transcription factors that can induce very profound changes as these are highly networked. For example, one or two single base pair mutations of the FoxP2 transcription factor gene have been linked to the development of human speech.
The Drosophila results from the Burke et al. work really confirm what most biomedical researchers already know. That is, many genes influence complex traits, and susceptibility to diseases does not arise from just a few genes. In the case of cancer, a gain of function of over 100 possible oncogenes and a loss of function of a similar number of tumour-suppressor genes are already well known to underlie neoplastic growth and metastasis. This is equally likely to be the case for most of the other major diseases of aging.
Nicholas Wade in his New York Times article suggests that if tens or hundreds of genes are involved in complex traits like disease susceptibility, then it may be close to impossible to develop effective treatments by the pharmaceutical industry. However, in an individual patient, it is actually only a few complementary mutations in a very small number of genes that actually give rise to most types of diseases. Therefore, if the defective proteins that are encoded by these genes are specifically targeted, then very successful outcomes can be produced in these patients. This is well exemplified by the use of Herceptin to treat about 10% of breast cancer patients that over-express the protein-tyrosine kinase receptor for epidermal growth factor. Similarly, Gleevec is very effective for treatment of many chronic myeloid leukemia patients that produce an overactive version of the protein-tyrosine kinase Abl. The pharmaceutical industry is well attuned to this and many new targeted drugs are already paving the way for personalized medicine.
Link to the original blog post.
At 25°C, the average Drosophila melanogaster can bred after about 8.5 days after birth, and in its life span of around 30 days lays about 400 eggs, usually 5 at a time. Human females are capable of reproduction usually from 12 years of age. However, historically in human societies, the average generation time appears to be about 20 years.
In the UC Irvine study by Burke et al., the genomes of the flies were analyzed after 600 generations with selective pressure for accelerated development. This would extrapolate to approximately 12,000 years in humans. As most researchers would have predicted, the increased rate of sexual development in the flies by selective breeding was due to the acquisition of mutations in many genes. Indeed, this supports the idea that "soft sweeps" underlie complex traits. However, it is also well appreciated that occasionally mutations can arise in genes that encode key regulatory proteins such as kinases and transcription factors that can induce very profound changes as these are highly networked. For example, one or two single base pair mutations of the FoxP2 transcription factor gene have been linked to the development of human speech.
The Drosophila results from the Burke et al. work really confirm what most biomedical researchers already know. That is, many genes influence complex traits, and susceptibility to diseases does not arise from just a few genes. In the case of cancer, a gain of function of over 100 possible oncogenes and a loss of function of a similar number of tumour-suppressor genes are already well known to underlie neoplastic growth and metastasis. This is equally likely to be the case for most of the other major diseases of aging.
Nicholas Wade in his New York Times article suggests that if tens or hundreds of genes are involved in complex traits like disease susceptibility, then it may be close to impossible to develop effective treatments by the pharmaceutical industry. However, in an individual patient, it is actually only a few complementary mutations in a very small number of genes that actually give rise to most types of diseases. Therefore, if the defective proteins that are encoded by these genes are specifically targeted, then very successful outcomes can be produced in these patients. This is well exemplified by the use of Herceptin to treat about 10% of breast cancer patients that over-express the protein-tyrosine kinase receptor for epidermal growth factor. Similarly, Gleevec is very effective for treatment of many chronic myeloid leukemia patients that produce an overactive version of the protein-tyrosine kinase Abl. The pharmaceutical industry is well attuned to this and many new targeted drugs are already paving the way for personalized medicine.
Link to the original blog post.