The origin of species and the selfish gene
Advances in genetics and developmental biology in the last five decades have challenged us to think about the role of genes preparing the species against the challenges of the environment. Biologist Richard Dawkins coins the metaphor “selfish gene” to suggest that genes are tempered by their need to keep their carrier species successful in nature, which is fundamental to its survival in the evolutionary process.
A brief summary of the book is as follows: Dawkins argues that the evolutionary concept of Natural Selection chooses specific sets of genes that confer the individual species to behave altruistically. For example, family and social behavior of feeding and protecting a social structure is common among species that share copies of the same genes. Within each individual species, some leave more “fit” offspring that contain some inheritable traits (genes). This non-random differential reproduction of genes is referred to as Natural Selection. A gene by cooperating with group if successful companion gene pools build a mortal machine that survives through a finite time. And all phenotypic effects, a set of observable characteristics of an individual resulting from an interaction of its genotype with its environment is present in an individual body. Genes have different functions; some genes are workers, some builders, while others manage the operation as a whole. This helps us understand the complex genetic networks regulating metabolism, reproduction and development. The gene pools give an inside look at the intricate and often surprising adaptations among species. The genetics of immune systems, the evolutionary benefits of sexual reproduction, and genetic differences among human populations are few examples of adaptation and natural selection. For example, humans and chimpanzee share about 99% of their evolutionary history. But how is that humans claim to be more “evolved” than chimpanzees? How did they acquire bigger brains?
A comparison of the DNA of chimpanzees and humans showed that a single letter change in the DNA of one gene triggered an increase in a population of stem cells called basal radial glia. These cells are thought to have powered the expansion of the human cerebral cortex. It also seems that chunks of DNA in the human had acquired “back-up copies” of particular genes, That made them ripe for some evolutionary tinkering; if the copy happens to acquire a few coding errors, there’s no problem, there’s still the functioning original. Once in a while however, a copying error might lead to a new function that is useful. A closer look at a duplicated human gene named SRGAP2C is a slightly altered in humans, but the unaltered original gene is found in chimps but the human SRGAP2C, delayed the maturation of neurons so spines kept sprouting, which enabled them to make more connections. Neurons develop and they acquire spines that act like antennae for receiving messages from other neurons. But the spines stop sprouting once the neurons mature, but altered SRGAP2C, by delaying the maturation process help it to get big and develop more connections and increases the complexity of the brain as it happened in humans.
Another backup copy of a gene that is present in humans but absent from chimps called ARHGAP11B caused a particular population of brain stem cells – basal radial glia – to increase their rounds of multiplication and grow bigger. The altered FOXP2 gene, unique to humans is responsible for turning thoughts into speech, but the unaltered genome is present in chimps where this evolutionary behavior is absent.
This book is 548 pages long and contains very little biological or genetic data. It is written for general readers that require no significant knowledge in evolutionary biology.
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