摘要:

Summary1Previous attempts to explain the evolution of spider silk have relied heavily on conjecture. The formulation of testable historical hypotheses to replace such speculation is discussed.2The importance of phylogenetic reconstructions and other historical hypotheses for use in generating and testing hypotheses concerning the evolution of specific adaptations is examined. Recent ideas on arachnid phylogeny are reviewed and their relevance to the problem of silk evolution in spiders is explored.3Evidence from the analysis of three historical problems (origin of spinnerets, origin of silk glands, original selective pressure favouring evolution of silk) is reviewed from three different frames of reference (in‐group analysis, out‐group analysis, convergence analysis). Several lines of evidence are found which suggest that silk use originated in spiders due to selective pressures associated with reproduction (specifically, the transfer of sperm or the protection of eggs).4The prevalence of segmental appendages retained for use in manipulating genital products in both arachnids and non‐arachnid arthropods and the probable placement of spinnerets near the genital opening in ancestral spiders suggest that spinnerets represent modified gonopods.5The most primitive types of silk glands are retained in virtually all spiders, in part, for use in the construction of sperm webs and egg sacs. Similar silk glands are found near the genital opening in many male spiders and used in building a portion of the sperm web.6The silk of adult arthropods other than spiders is used largely in manipulating or protecting sex cells. If there are multiple functions, use in reproduction is typically one of them. Thus, there is evidence for strong selective pressure favouring the evolution of silk for use in reproduction.7Two hypotheses are proposed which are consistent with the conclusion that silk in spiders evolved for reproductive needs (the spermatophore‐sperm web and egg sac hypotheses). Testable predictions of each hypothesis are p

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1987.tb01263.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

SummaryCell selection is recognized to be the principal mechanism in the generation of the immune response. The role of cell selection in other developmental systems is considered here, with emphasis on the morphogenesis of the vertebrate limb, the formation of pigment pattern in the pelt of mammals and the changes that occur in the human erythrocyte at the time of birth.

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1987.tb01264.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

Summary1To answer the question ‘What controls the rate of respiration?’ requires a clear definition of control and an explicit description of the limits of the system to be considered. In this review we use a neutral definition of control in whichAcontrolsBif changes inAcause changes inB.A useful system to define when discussing the control of respiration consists of the electron transport chain, the H+‐ATPase, the adenine nucleotide carrier, the intramitochondrial adenine nucleotide and phosphate pools, δpand the proton leak across the mitochondrial inner membrane.2Controls operating within this system are designated internal controls and many of them are fairly well characterized. Several models have been advanced to describe the rates of these internal processes in isolated mitochondria, including control of respiration rate by cytochrome oxidase with all other steps near to equilibrium, control by the adenine nucleotide carrier or control by the extent of displacement of individual reactions from equilibrium. More recently, analysis using control theory has shown that in the resting state (state 4) most control over flux is exerted by the leak of protons through the inner membrane, whereas in more active, phosphorylating states (up to state 3) control is distributed between a number of steps, including the proton leak, the adenine nucleotide carrier and cytochrome oxidase. This approach seems a very useful framework within which to pose further questions.3This system may be treated as a ‘black box’ interacting with its environment (the rest of the mitochondrion and the experimental cuvette or living cell) through the redox states of NAD, Q and O2and through the phosphorylation state of the extramitochondrial adenine nucleotides. Very few external effectors cross the system boundary; the only well‐characterized ones are long‐chain fatty acyl‐CoA, which inhibits the adenine nucleotide carrier, and fatty acids, which activate a specific uncoupling protein found only in the inner membrane of mitochondria from brown adipose tissue. At this level respiration rate is determined only by the internal properties of the ‘black box’, by the redox states of NAD, Q and O2, and by the phosphorylation status of the extramitochondrial adenine nucleotide pool.4Within a cell the rate of respiration is controlled primarily by the rates of reactions feeding electrons to the electron transport chain (through their effects on NADH/NAD and QH2/Q ratios) and by the rates of reactions consuming or producing ATP (through the cytosolic phosphorylation potential or ATP/ADP ratio). Control of reducing equivalent supply occurs through availability of oxidizable substrates (determined by diet and hormonal status), through regulation of pathways such as glycolysis or fatty acid catabolism and, importantly, through Ca2+activation of intramitochondrial dehydrogenases.5Hormonal control over respiration can occur at all the levels mentioned. Hormones may alter the kinetic properties of the oxidative phosphorylation system by altering the concentrations of individual proteins or by altering their kinetic properties either by affecting the lipid environment or, possibly, more directly. Important controls by hormones occur through changes in ATP demand altering the cytoplasmic adenine nucleotide pool and by changes in free Ca2+concentration in the mitochondrial matrix, altering the activity of dehydrogenases and the supply of electrons to NAD and Q. Hormones also affect the supply of reducing equivalents to the mitochondria by their catabolic or anabolic effec

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1987.tb01265.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1987.tb01266.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY