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Two costs of sexual reproduction are commonly recognized: the cost of recombination and the cost of producing sons, also referred to as the cost of meiosis. In addition, there are also the costs incurred in finding and fertilizing a mate.
Summary of Section 4.4
To offset these costs, sexual reproduction must also confer benefits if it is to persist. Two types of benefits have been discussed: long-term benefits associated with more rapid evolution of species or populations, and shortterm benefits to individuals.
Summary of Section 4.4
Rapid evolution of species or populations in the long term may be facilitated by the more rapid fixation of combinations of advantageous mutations in sexual populations or by the reassembly, by recombination, of mutation-free genotypes (a solution to Muller’s ratchet).
Summary of Section 4.4
There are several theories about why sex arises and persists in the short term. They rely primarily on the advantage of sex to individuals in a changing environment. Some theories focus on changes in the organism’s physical environment (sib-competition model, lottery model) whereas others focus on changes in the biological environment (Red Queen hypothesis).
Summary of Section 4.4
Male and female sexes are defined by the difference in the size of their gametes. The prevalent theory holds that distinct sexes evolved because it is advantageous, on the one hand, to produce numerous gametes (sperm) and,
proportion of males
on the other, to produce large gametes (eggs) because the zygote’s survival is
(d)
20 30
enhanced by large size.
Summary of Section 4.5
The sex ratio is usually 1 : 1 because the reproductive success of all males in a population must equal the reproductive success of all females. If the population sex ratio deviates from 1: 1, natural selection favours individuals that produce more offspring of the rarer sex.
Summary of Section 4.5
Biases away from a 1 : 1 sex ratio do occur in nature, either as a result of manipulation of primary sex ratios or because of unequal investment in the two sexes in offspring that require parental care.
Summary of Section 4.5
There are two major categories of sex determination: genetic and environmental.Within these categories, there are many contrasting mechanisms that differ even in quite closely related groups.
Summary of Section 4.5
There are two kinds of hermaphrodites, simultaneous and sequential. Simultaneous hermaphrodites may or may not be capable of self-fertilization.
Summary of Section 4.6
Some animals and plants switch sex once during their lifetime, from male to female, or vice versa.Whether it is advantageous to begin as one sex or the other depends on how reproductive success as a male or as a female changes with an individual’s size or age.
Summary of Section 4.6
Host species throughout the animal kingdom have evolved complex arrays of defences against pathogens, which include physical barriers, reflexes such as coughing and behaviours such as grooming. If these barriers are breached, then the first (and in invertebrates, the only) defence against pathogens is the molecular and cellular mechanisms known as innate immunity.
Summary of Section 5.2
Innate immune defences pre-exist in the host animal before it comes into contact with pathogens for the first time; constitutive defences are permanently activated whereas induced defences increase locally or exist in a precursor form and are activated by the presence of pathogens.
Summary of Section 5.2
Molecular defences include wound closure and coagulation, agglutination of pathogens, antimicrobial peptides and enzymes, oxidizing chemicals and other toxic molecules, pore-forming proteins that puncture cell membranes, and molecules that interfere with pathogen replication. Some of these molecules are generated in induced cascade reactions.
Summary of Section 5.2
Cellular defences involve different types of leukocytes: some destroy pathogens by phagocytosis, others engage in cell-mediated cytotoxicity, and collectively they synthesize and secrete many of the molecular defences listed above.
Summary of Section 5.2
Many of the genes for molecules involved in innate immunity are highly conserved between widely divergent animal phyla, which may indicate a common origin in shared ancestors.
Summary of Section 5.2
Innate immunity relies on broad-spectrum defensive mechanisms, which are targeted against unique pathogen carbohydrates commonly found in the surface structures of pathogens. Innate immune mechanisms are non-specifically effective against all pathogens that contain these molecules.
Summary of Section 5.2
The effectiveness of the innate immune response to invasion by a particular pathogen is more-or-less constant, no matter how many times the same pathogen is encountered (i.e. it does not adapt during an exposure).
Summary of Section 5.2
Innate defences are self-tolerant and are not directed against the host’s own cells unless they betray the presence of intracellular pathogens. Unique histocompatibility antigens on host cells are recognized as ‘non-self’ if grafted into another member of the same species, provoking graft rejection.
Summary of Section 5.2
Plants have evolved a wide range of physical and chemical defence mechanisms, in response to a variety of herbivores and pathogens. Interactions between some groups of herbivorous insect and plant species have occurred over tens of millions of years.
Summary of Section 5.3
The plant apparency theory and the resource availability hypothesis can explain the diversity of plant chemical defences, i.e. why certain plant species have different types and amounts of defence, leading to the idea of qualitative and quantitative defences.
Summary of Section 5.3
Alkaloids are important plant secondary compounds implicated in defence against a range of herbivores and pathogens. The plant defence theory was the first to suggest the defence role of secondary chemicals like alkaloids.
Summary of Section 5.3
Induced defence, an example of a qualitative defence, has been found in various plant species. The principles of the mechanisms, in particular the cascade response, are similar to those in animals.
Summary of Section 5.3
Adaptive immunity is found only in vertebrates and depends on small lymphocytes, which exist in clones initially of a few hundred cells each. All members of the same clone carry identical antigen receptors with binding sites that fit a unique cluster of amino acids (sometimes with sugar molecules) called an epitope.
Summary of Section 5.4
Molecules with epitopes in their structure are called antigens. The antigen receptors on small lymphocytes are highly specific and can distinguish between closely related pathogen strains on the basis of their unique epitopes.
Summary of Section 5.4
In most vertebrates, large antigen receptor repertoires are generated by random somatic gene recombination. Somatic genes are not passed on from one generation to the next, so the codes for receptors that bind to epitopes on pathogens encountered during an animal’s lifetime are not inherited by its offspring.
Summary of Section 5.4
Phagocytes also produce activating cytokines and select appropriate targets for adaptive immunity by presenting digested fragments of pathogens to helper T cells.
Summary of Section 5.4
Corticosteroids suppress immune responses and may be important in switching energy resources away from defence against pathogens to other functions such as reproduction, metamorphosis and hibernation.
Summary of Section 5.4
Some amphibian populations may be declining due to increased mortality from pathogens. Increased susceptibility to opportunistic infections may be due to reduced immune responsiveness caused by environmental stressors, or to the recent emergence of more virulent pathogen strains.
Summary of Section 5.4
There are several lines of evidence to show that organisms involved in attack and defence have coevolved and that trade-offs are occurring between devoting resources to defence or to other functions such as reproduction.
Summary of Section 5.5
A consequence of coevolution between hosts and their pathogens is that virulence tends towards an optimum level which ensures the survival of both the host and the pathogen species. Hosts may tolerate a greater pathogen load during periods of high reproductive effort.
Summary of Section 5.5
Comparison of the phylogenies of hosts and parasites provide further evidence for coevolution. Blood parasites in the order Haemosporina seem to have coevolved with their dipteran (fly) vectors rather than their vertebrate hosts.
Summary of Section 5.5
Coevolution of some plants and insect herbivores has led to the latter using the plants’ defence for themselves, which in turn has contributed to the evolution of warning coloration and mimicry.
Summary of Section 5.5
Experimental evidence for coevolution in plants and herbivores has come from a study in which the removal of herbivores was associated with increased fitness of plants, due to the reduced cost of defence.
Summary of Section 5.5
Longevity is difficult to measure in wild animals and values for captive specimens may not be representative.
Summary of Sections 6.1 and 6.2
Survival plots summarize the mortality pattern of a particular species. Those of closely related species can differ greatly.
Summary of Sections 6.1 and 6.2
Ageing (senescence) is an intrinsic cause of death; extrinsic factors from the environment include starvation, disease, predation and accidents.
Summary of Sections 6.1 and 6.2
Organisms that produce many offspring at an early age have shorter lives than similar species that delay reproduction, i.e. there is a trade-off between longevity and reproduction.
Summary of Sections 6.1 and 6.2
Life histories can be characterized as mixtures of properties that maximize population growth rate or carrying capacity.
Summary of Section 6.3
Theory predicts that long-lived iteroparous organisms can increase their fitness by limiting or delaying reproduction in early life. In species in which reproductive success is strongly correlated with body size, breeding may be delayed until large body size has been achieved.
Summary of Section 6.3
A cost of delayed breeding is a reduced probability of surviving to breed at all. In some species, these effects have led to marked differences in the life history and longevity of males and females.
Summary of Section 6.3
Observational and experimental evidence reveal a trade-off between survival and reproduction: the energetic and other costs of reproduction reduce annual survival and thus longevity.
Summary of Section 6.3
As individual animals get older, they acquire skills that increase their reproductive success, and they invest more in reproduction; however, in older individuals these effects are countered by reproductive senescence.
Summary of Section 6.3
Within their lifespan, organisms may limit their reproductive effort in one year and so increase their reproductive success in subsequent years.
Summary of Sections 6.3
Longevity and reproductive strategy vary within a species as well as
differing between species. Some of the differences are genetic.
Summary of Sections 6.4 and 6.5
Artificial selection for longevity in short-lived laboratory animals increases
mean lifespan by as much as twofold.
Summary of Sections 6.4 and 6.5
Frequent experience of internal fertilization per se, as well as the trade-off
between body maintenance and egg production, reduce the lifespan of
females that breed.
Summary of Sections 6.4 and 6.5
In some animals, there is a trade-off between reproductive success and immune function.
Summary of Sections 6.6 and 6.7
Secondary sexual characters may indicate a male’s capacity to resist parasites and pathogens.
Summary of Sections 6.6 and 6.7
Salmon have two alternative life histories determined in part by genes but also by growth and social status early in life.
Summary of Sections 6.6 and 6.7
A few other long-lived mammals as well as humans undergo menopause, a post-reproductive state about whose adaptive significance several hypotheses have been proposed.
Summary of Sections 6.6 and 6.7
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