Richard Dawkins Selfish Gene Book Pdf Download
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If you haven't found the information you require from our website, please contact us by calling or emailing us at enquiries bolton. If you haven't found the information you require from our website, please contact us by calling or emailing us at international bolton. This summary omits reference to Chapter 3 'Arguments for God's Existence' as there have been many critiques of these arguments from believers and non-believers.
- Richard Dawkins The Selfish Gene
- The 100 best nonfiction books: No 10 – The Selfish Gene by Richard Dawkins
- Richard Dawkins
- Richard Dawkins The Selfish Gene
Richard Dawkins The Selfish Gene
Selfish genetic elements historically also referred to as selfish genes, ultra-selfish genes, selfish DNA, parasitic DNA, genomic outlaws are genetic segments that can enhance their own transmission at the expense of other genes in the genome, even if this has no or a negative effect on organismal fitness. However, when genes have some control over their own transmission, the rules can change, and so just like all social groups, genomes are vulnerable to selfish behaviour by their parts.
Early observations of selfish genetic elements were made almost a century ago, but the topic did not get widespread attention until several decades later. Both papers emphasized that genes can spread in a population regardless of their effect on organismal fitness as long as they have a transmission advantage.
Selfish genetic elements have now been described in most groups of organisms, and they demonstrate a remarkable diversity in the ways by which they promote their own transmission.
PLoS Genet 14 11 : e This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Wing, M. Long and AGC. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing interests: The authors have declared that no competing interests exist. Observations of what we now refer to as selfish genetic elements go back to the early days in the history of genetics. Already in , Russian geneticist Sergey Gershenson reported the discovery of a driving X chromosome in Drosophila obscura.
They need only be useful to themselves. Around the same time, several other examples of selfish genetic elements were reported. For example, the American maize geneticist Marcus Rhoades described how chromosomal knobs led to female meiotic drive in maize. Viewing evolution as a struggle between competing replicators made it easier to recognize that not all genes in an organism would share the same evolutionary fate. In , two high profile papers published back-to-back in Nature by Leslie Orgel and Francis Crick , and Ford Doolittle and Carmen Sapienza respectively, brought the study of selfish genetic elements to the centre of biological debate.
The two papers led to a series of exchanges in Nature. If the Selfish DNA papers marked the beginning of the serious study of selfish genetic elements, the subsequent decades have seen an explosion in theoretical advances and empirical discoveries.
Leda Cosmides and John Tooby wrote a landmark review about the conflict between maternally inherited cytoplasmic genes and biparentally inherited nuclear genes.
Then in , John H. Werren and colleagues wrote the first major empirical review of the topic. First, it coined the term selfish genetic element, putting an end to a sometimes confusingly diverse terminology selfish genes, ultra-selfish genes, selfish DNA, parasitic DNA, genomic outlaws.
Second, it formally defined the concept of selfish genetic elements. Finally, it was the first paper to bring together all different kinds of selfish genetic elements known at the time genomic imprinting, for example, was not covered. In the late s, most molecular biologists considered selfish genetic element to be the exception, and that genomes were best thought of as highly integrated networks with a coherent effect on organismal fitness. In , when Austin Burt and Robert Trivers published the first book-length treatment of the topic, a comprehensive piece that remains the go-to source on the topic, the tide was changing.
While their role in evolution long remained controversial, in a recent review, a century after their first discovery, William R. Though selfish genetic elements show a remarkable diversity in the way they promote their own transmission, some generalizations about their biology can be made. In a classic review, Gregory D. Hurst and John H. Sexual reproduction involves the mixing of genes from two individuals. Highly self-fertilizing or asexual genomes are expected to experience less conflict between selfish genetic elements and the rest of the host genome than outcrossing sexual genomes.
First, sex and outcrossing put selfish genetic elements into new genetic lineages. In contrast, in a highly selfing or asexual lineage, any selfish genetic element is essentially stuck in that lineage, which should increase variation in fitness among individuals. Second, the increased homozygosity in selfers removes the opportunity for competition among homologous alleles. Third, theoretical work has shown that the greater linkage disequilibrium in selfing compared to outcrossing genomes may in some, albeit rather limited, cases cause selection for reduced transposition rates.
One caveat to this is that the evolution of selfing is associated with a reduction in the effective population size. Empirical evidence for the importance of sex and outcrossing comes from a variety of selfish genetic elements, including transposable elements,[ 36 , 37 ] self-promoting plasmids,[ 38 ] and B chromosomes.
The presence of selfish genetic elements can be difficult to detect in natural populations. Instead, their phenotypic consequences often become apparent in hybrids. The first reasons for this is that some selfish genetic elements rapidly sweep to fixation, and the phenotypic effects will therefore not be segregating the in the population.
Hybridization events, however, will produce offspring with and without the selfish genetic elements and so reveal their presence. The second reason is that host genomes have evolved mechanisms to suppress the activity of the selfish genetic elements, for example the small RNA administered silencing of transposable elements.
Hybrid offspring, on the other hand, may inherit a given selfish genetic element, but not the corresponding suppressor and so reveal the phenotypic effect of the selfish genetic element. Some selfish genetic elements manipulate the genetic transmission process to their own advantage, and so end up being overrepresented in the gametes Fig 2.
Such distortion can occur in various ways, and the umbrella term that encompasses all of them is segregation distortion. Some elements can preferentially be transmitted in egg cells as opposed to polar bodies during meiosis, where only the former will be fertilized and transmitted to the next generation.
Any gene that can manipulate the odds of ending up in the egg rather than the polar body will have a transmission advantage, and will increase in frequency in a population.
Segregation distortion can happen in several ways. When this process occurs during meiosis it is referred to as meiotic drive. Many forms of segregation distortion occur in male gamete formation, where there is differential mortality of spermatids during the process of sperm maturation or spermiogenesis. When segregation distortion acts on sex chromosomes, they can skew the sex ratio. One example is the lethality of the t-haplotype in mice,[ 51 ]another is the effect on male fertility of the Sex Ratio system in D.
A phenomenon closely related to segregation distortion is homing endonucleases. Homing endonucleases insert themselves into the genome at the site homologous to the first insertion site, resulting in a conversion of a heterozygote into a homozygote bearing a copy of the homing endonuclease on both homologous chromosomes Fig 3.
This gives homing endonucleases an allele frequency dynamics rather similar to a segregation distortion system, and generally unless opposed by strong countervailing selection, they are expected to go to fixation in a population. This converts a heterozygote into a homozygote. Transposable elements TEs include a wide variety of DNA sequences that all have the ability to move to new locations in the genome of their host.
Transposons do this by a direct cut-and-paste mechanism, whereas retrotransposons need to produce an RNA intermediate to move. TEs were first discovered in maize by Barbara McClintock in the s[ 17 ] and their ability to occur in both active and quiescent states in the genome was also first elucidated by McClintock. Most random insertions into the genome appear to be relatively innocuous, but they can disrupt critical gene functions with devastating results.
Both plant and animal hosts have evolved means for reducing the fitness impact of TEs, both by directly silencing them and by reducing their ability to transpose in the genome. The fitness of a TE is a combination of its ability to expand in numbers within a genome, to evade host defences, but also to avoid eroding host fitness too drastically.
The effect of TEs in the genome is not entirely selfish. Because their insertion into the genome can disrupt gene function, sometimes those disruptions can have positive fitness value for the host. Many adaptive changes in Drosophila [ 62 ] and dogs[ 63 ] for example, are associated with TE insertions.
B chromosomes refer to chromosomes that are not required for the viability or fertility of the organism, but exist in addition to the normal A set. They often vary in copy number between individuals of the same species. Examples include cytoplasmic male sterility see Selfish mitochondria.
While mitochondrial and chloroplast genes are generally maternally inherited, B chromosomes can be preferentially transmitted through both males and females. B chromosomes were first detected over a century ago. B chromosome number correlates positively with genome size[ 67 ] and has also been linked to a decrease in egg production in the grasshopper Eyprepocnemis plorans.
Genomic conflicts often arise because not all genes are inherited in the same way. Probably the best example of this is the conflict between uniparentally usually but not always, maternally inherited mitochondrial and biparentally inherited nuclear genes.
Indeed, one of the earliest clear statement about the possibility of genomic conflict was made by the English botanist Dan Lewis in reference to the conflict between maternally inherited mitochondrial and biparentally inherited nuclear genes over sex allocation in hermaphroditic plants Fig 5. A single cell typically contains multiple mitochondria, creating a situation for competition over transmission.
Uniparental inheritance been suggested to be a way to reduce the opportunity for selfish mitochondria to spread, as it ensures all mitochondria share the same genome, thus removing the opportunity for competition.
The conflict between mitochondrial and nuclear genes is especially easy to study in flowering plants. Mitochondrial genes are typically only transmitted through female gametes, and therefore from their point of view the production of pollen leads to an evolutionary dead end. Any mitochondrial mutation that can affect the amount of resources the plant invests in the female reproductive functions at the expense of the male reproductive functions improves its own chance of transmission. Cytoplasmic male sterility is the loss of male fertility, typically through loss of functional pollen production, resulting from a mitochondrial mutation.
The co-evolutionary arms race between selfish mitochondrial genes and nuclear compensatory alleles can often be detected by crossing individuals from different species that have different combinations of male sterility genes and nuclear restorers, resulting in hybrids with a mismatch. Another consequence of the maternal inheritance of the mitochondrial genome is the so-called Mother's Curse.
Another sort of conflict that genomes face is that between the mother and father competing for control of gene expression in the offspring, including the complete silencing of one parental allele.
Due to differences in methylation status of gametes, there is an inherent asymmetry to the maternal and paternal genomes that can be used to drive a differential parent-of-origin expression. Imprinting seems like a maladaptive phenomenon, since it essentially means giving up diploidy, and heterozygotes for one defective allele are in trouble if the active allele is the one that is silenced.
Several human diseases, such as Prader-Willi and Angelman syndromes, are associated with defects in imprinted genes. The asymmetry of maternal and paternal expression suggests that some kind of conflict between these two genomes might be driving the evolution of imprinting. In particular, several genes in placental mammals display expression of paternal genes that maximize offspring growth, and maternal genes that tend to keep that growth in check Fig 6.
Many other conflict-based theories about the evolution of genomic imprinting have been put forward. In mice, the insulin-like growth factor 2 gene, Igf2 , which is linked to hormone production and increased offspring growth is paternally expressed maternally silenced and the insulin-like growth factor 2 receptor gene Igf2r , which binds the growth protein and so slows growth, is maternally expressed paternally silenced.
The offspring is normal sized when both genes are present, or both genes are absent. When the maternally expressed gene Igf2r is experimentally knocked out the offspring has an unusually large size, and when the paternally expressed gene Igf2 is knocked out, the offspring is unusually small. At the same time, genomic or sexual conflict are not the only possible mechanisms whereby imprinting can evolve.
An important point to note regarding genomic imprinting is that it is quite heterogeneous, with different mechanisms and different consequences of having single parent-of-origin expression.
For example, examining the imprinting status of closely related species allows one to see that a gene that is moved by an inversion into close proximity of imprinted genes may itself acquire an imprinted status, even if there is no particular fitness consequence of the imprinting. A greenbeard gene is a gene that have the ability to recognize copies of itself in another individuals and then make its carrier act preferentially toward such individuals.
The 100 best nonfiction books: No 10 – The Selfish Gene by Richard Dawkins
Selfish genetic elements historically also referred to as selfish genes, ultra-selfish genes, selfish DNA, parasitic DNA, genomic outlaws are genetic segments that can enhance their own transmission at the expense of other genes in the genome, even if this has no or a negative effect on organismal fitness. However, when genes have some control over their own transmission, the rules can change, and so just like all social groups, genomes are vulnerable to selfish behaviour by their parts. Early observations of selfish genetic elements were made almost a century ago, but the topic did not get widespread attention until several decades later. Both papers emphasized that genes can spread in a population regardless of their effect on organismal fitness as long as they have a transmission advantage. Selfish genetic elements have now been described in most groups of organisms, and they demonstrate a remarkable diversity in the ways by which they promote their own transmission. PLoS Genet 14 11 : e
W hat is man, and what are we for? Remarkably, it was not until Charles Darwin published On the Origin of Species in that anyone, in our history, had thought methodically to address the reason for our existence. A hundred years later, in the heady, innovative atmosphere of the s, a new generation of young and ambitious evolutionary biologists found themselves confronted with a rare opportunity: the rediscovery and renewal of evolutionary theory. Enter Richard Dawkins, a young Oxford zoologist who had been born, and partly raised, in Africa. It is the gene, the unit of heredity.
Полностью отключив электроснабжение, они могли бы остановить работу ТРАНСТЕКСТА, а вирус удалить позже, просто заново отформатировав жесткие диски компьютера. В процессе форматирования стирается память машины - информация, программное обеспечение, вирусы, одним словом - все, и в большинстве случаев переформатирование означает потерю тысяч файлов, многих лет труда. Но ТРАНСТЕКСТ не был обычным компьютером - его можно было отформатировать практически без потерь. Машины параллельной обработки сконструированы для того, чтобы думать, а не запоминать.
По вашему приказу, директор, - говорил он, - мы провели в Севилье два дня, выслеживая мистера Энсея Танкадо. - Расскажите, как он погиб, - нетерпеливо сказал Фонтейн. Смит сообщил: - Мы вели наблюдение из мини-автобуса с расстояния метров в пятьдесят.
Richard Dawkins The Selfish Gene
Интуиция подсказывала ему, что в глубинах дешифровального чудовища происходит что-то необычное. ГЛАВА 10 - Энсей Танкадо мертв? - Сьюзан почувствовала подступившую к горлу тошноту. - Вы его убили.
Расстрельная камера, мысленно усмехнулся. Халохот оценил расстояние до входа. Семь ступеней.
Стратмор даже не пошевелился. - Коммандер. Нужно выключить ТРАНСТЕКСТ. У нас… - Он нас сделал, - сказал Стратмор, не поднимая головы. - Танкадо обманул всех. По его тону ей стало ясно, что он все понял. Вся ложь Танкадо о невскрываемом алгоритме… обещание выставить его на аукцион - все это было игрой, мистификацией.
PDF | The thirtieth anniversary of Richard Dawkins' landmark work provides an Download full-text PDF 30 years ago, The Selfish Gene has been, and. remains, one of the most influential science. books of all time.
The Selfish Gene
Шифруя послание, Сьюзан просто заменила в нем каждую букву на предшествующую ей алфавите. Для расшифровки Беккеру нужно было всего лишь подставить вместо имеющихся букв те, что следовали непосредственно за ними: А превращалось в В, В - в С и так далее. Беккер быстро проделал это со всеми буквами. Он никогда не думал, что четыре слова могут сделать его таким счастливым: IM GLAD WE MET Что означало: Я рада, что мы встретились. Он быстро нацарапал на программке ответ и протянул Сьюзан: LDSNN Сьюзан, прочитав, просияла. ME TOO, что означало: Я .
- Он покачал головой, словно не веря такую удачу. - Чертовское везение, если говорить честно. - Он, казалось, все еще продолжал сомневаться в том, что Хейл оказался вовлечен в планы Танкадо. - Я полагаю, Хейл держит этот пароль, глубоко запрятав его в компьютере, а дома, возможно, хранит копию. Так или иначе, он попал в западню. - Тогда почему бы не вызвать службу безопасности, которая могла бы его задержать.
Стандартная для АНБ процедура. Мне нужно знать, с кем я имею .
Но вместо признаков срыва Фонтейн обнаружил подготовительную работу над беспрецедентной разведывательной операцией, которую только можно было себе представить. Неудивительно, что Стратмор просиживает штаны на работе. Если он сумеет реализовать свой замысел, это стократно компенсирует провал Попрыгунчика.
Вот где кольцо! - подумал. - В сумке. - и улыбнулся, едва сохраняя спокойствие.
Прозвучал еще один выстрел. Он принял решение. Под визг покрышек, в снопе искр Беккер резко свернул вправо и съехал с дороги. Колеса мотоцикла подпрыгнули, ударившись о бетонное ограждение, так что он едва сумел сохранить равновесие.
- Что еще мне остается? - Он представил Хейла на скамье подсудимых, вываливающего все, что ему известно о Цифровой крепости.