摘要:

SUMMARY1Both laboratory and wild house mice,Mus musculus, given bedding, can breed in captivity in an environment kept at – 3°C. The nest temperature when a young litter is present then fluctuates widely. In a typical laboratory (at 21°C) the temperature of the nest is both higher and more constant.2The ovaries of pregnant mice breeding at – 3°C have more corpora lute a than controls at 21°C. This is not an index of a higher ovulation rate, but is evidently due to the presence of corpora lutea from a pievious ovulation.3In the absence of concurrent lactation, weights and numbers of foetuses at the sixteenth day of gestation are little affected by cold; but in both environments foetal weight diminishes with increasing size of litter. This is a systemic effect: foetal weight is hardly if at all influenced by the number of other foetuses in the same uterine horn.4Cold delays the onset of breeding and lengthens the interval between litters. Mean litter sizes are usually lower than in the warm environment, mainly through absence of large litters.5The body weights of laboratory mice are usually lower at – 3°C than 21°C at all ages from 3 weeks. This does not, however, apply to strain C57BL, which never stores much fat in adipose tissue. Wild mice bred at – 3°C are heavier than controls at 21°C, possibly because only the heavier individuals survive in early life.6F1hybrids produced by crossing two inbred strains breed better and more consistently than the parent strains at both temperatures; but the effect of heterozygosis is much greater in the cold environment.7Food intake changes little during pregnancy, but rises greatly during the first 10 days of lactation at both temperatures.8At 21°C, body weight, excluding the weight of the litter, increases only slightly during pregnancy; but the weights of the heart and liver are greatly increased. The weight of the stomach also rises; the small intestine lengthens, but becomes lighter. During lactation the liver becomes still heavier, and the small intestine more than restores its loss of weight. The kidneys also become heavier. At – 3°C similar changes occur, but the heart is heavier at all stages of the reproductive cycle than it is at 21°C. The kidneys, too, are consistently heavier in the cold, and so is the small intestine. By contrast, the liver of pregnant or lactating females at – 3°C is no heavier than in the warm environment.9Pregnancy entails an increase in the absolute amount of nitrogen in the body, in both environments; but females at – 3°C have less nitrogen and collagen than controls. Pregnancy does not alter body fat at either temperature, but lactation is accompanied by some loss. At birth, mice born in the cold environment have more than twice as much body fat as controls.10When mice are bred for their full reproductive span, the effect of a cold environment depends markedly on genotype. Mice of strain A2G/Tb eventually produce as many young in the cold environment as in the warm, but take longer to do so; C57BL/Tb produce fewer young, Wild mice produce fewer litters at – 3°C, and have a much higher nestling mortality. Most of the mortality is due to loss of whole litters.11The preceding statements apply to mice of the first two or three generations in a cold environment, There are further effects of breeding for many generations in the cold. Wild mice bred for ten generations lose fewer litters in later than in earlier generations. After ten generations, some wild mice were moved from –3 to 21°C. Their reproductive performance was then much superior to that of controls which had been kept at 21°C throughout. The transferred mice were also quicker than the controls to make a nest of paper.12Genetically heterogeneous laboratory mice, after twelve generations in the cold, were similarly returned to the warm environment. Their offspring were heavier than controls; but there was no superiority in reproductive performance.13A2G/Tb mice kept at –3°C, though highly inbred, also improved in reproductive performance over a number of generations: in particular, their infant mortality declined. This was probably not due to a genetical change, but to a cumulative maternal effect.14Maternal performance was studied by cross‐fostering young at birth between these ‘Eskimo’ mice, ‘immigrant’ mice of the first or second generation reared in the cold, and controls at 21°C. There was some evidence of an effect of true parentage, regardless of foster parentage, on body weight: the young of the Eskimo mice tended to be heavier than the others. There was also evidence that this influence persisted into a second generation. Mortality among the fostered young was influenced only by true parentage, not by foster parentage or environmental temperature. Some of the fostered mice were mated. Again, among their young, mortality in the nest was not affected by environmental temperature; but those whose true ancestry was Eskimo displayed a lower mortality than the others.15If a young mammal is given special treatment (such as exposure outside the nest), the treatment may influence, not only the individual treated, but also the behaviour of the parents; and the altered parental behaviour may in turn affect the development of the young. Enhanced parental attention in the nest has been directly observed after young have been exposed to cold or other treatment. It can probably accelerate maturation, and improve reproductive performance by lowering mortality among the young of the treated mice. Hence the direct effects of treatment in infancy can never be distinguished with certainty from indirect effects through changed parental behaviour, unless the experimental animals are reared artificially.16A comprehensive theory of ‘stress’, that is, of the response of a species to an environmental change for the worse, requires that attention should be paid to the following: (i) the effects of physiological (ontogenetic) adaptation to one ‘stressor’, such as cold, on response to another, such as infection; (ii) the ways in which conditions of rearing, especially early exposure to mildly adverse conditions such as lower temperature, influence later physiological, reproductive and behaviour al performance; (iii) the relationships of the abo

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1973.tb01567.x

出版商:Blackwell Publishing Ltd    

年代:1973

数据来源: WILEY

摘要:

SUMMARY1Although much is known about the effects of plant hormones and their role in the control of growth and differentiation, little is known about the way in which hormone production is itself controlled or about the cellular sites of hormone synthesis. The literature on hormone production is discussed in this review in an attempt to shed some light on these problems.2The natural auxin of plants, indol‐3yl‐acetic acid (IAA) is produced by a wide variety of living organisms. In animals, fungi and bacteria it is formed as a minor by‐product of tryptophan degradation. The pathways of its production involve either the transamination or the decarboxylation of tryptophan. The transaminase route is the more important.3In higher plants auxin is also produced as a minor breakdown product of trypto phan, largely via transamination. In some species decarboxylation may occur but is of minor importance. Tryptophan can also be degraded by spontaneous reaction with oxidation products of certain phenols.4The unspecific nature of the enzymes involved in IAA production and the probable importance of spontaneous, nonenzymic reactions in the degradation of tryp to phan make it unlikely that auxin production from tryptophan can be regulated with any precision at the enzymic level. The limiting factor for auxin production is the availability of tryptophan, which in most cells is present in insufficient quantities for its degradation to occur to a significant extent. Tryptophan levels are, however, considerably elevated in cells in which net protein breakdown is taking place as a result of autolysis.5An indole compound, glucobrassicin, occurs inBrassicaand a number of other genera. It breaks down readily to form a variety of products including indole aceto‐nitrile, which can give rise to IAA. There is, however, no evidence to indicate that glucobrassicin is a precursor of auxinin vivo.6Conjugates of IAA, e.g. IAA‐aspartic acid and IAA‐glucose, are formed when IAA is supplied in unphysiologically high amounts to plant tissues. These and other IAA conjugates occur naturally in developing seeds and fruits. There is no persuasive evidence for the natural occurrence of IAA‐protein complexes.7Tissues autolysing during prolonged extraction with ether produce IAA from tryptophan released by proteolysis. IAA is produced in considerable quantities by autolysing tissuesin vitro.8During the senescence of leaves proteolysis results in elevated levels of trypto phan. Large amounts of auxin are produced by senescent leaves.9Coleoptile tips have a vicarious auxin economy which depends on a supply of IAA, IAA esters and other compounds closely related to IAA from the seed. These move acropetally in the xylem and accumulate at the coleoptile tip. The production of auxin in coleoptile tips involves the hydrolysis of IAA esters and the conversion of labile, as yet unidentified compounds, to IAA. There is no evidence for thede novosynthesis of IAA in coleoptiles.10Practically all the other sites of auxin production are sites of both meristematic activity and cell death. The production of auxin in developing anthers and fertilized ovaries takes place in the regressing nutritive tissues (tapetum, nucellus, endosperm) as the cells break down. In shoot tips, developing leaves, secondarily thickening stems, roots and developing fruits auxin is produced as a consequence of vascular differ entiation; the differentiation of xylem cells and most fibres involves a complete auto‐lysis of the cell contents; the differentiation of sieve tubes involves a partial autolysis. There is no evidence that meristematic cells produce auxin.11The lysis and digestion of cells infected with fungi and bacteria results in elevated tryptophan levels and the production of auxin. Viral infections reduce the levels of tryptophan and are asSociated with reduced levels of auxin.12Crown‐gall tissues produce auxin. It is suggested that the crown‐gall disease may involve at any given time the death of a minority of the cells which produce auxin and other hormones as they autolyse; the other cells grow and divide in response to these hormones.13Auxin is produced in soils, particularly those rich in decaying organic matter, by micro‐organisms. This environmental auxin may be important for the growth of roots.14There is no convincing evidence that auxin is a hormone in non‐vascular plants. The induction of rhizoids in liverworts by low concentrations of auxin can be ex plained as a response to environmental auxin.15Abscisic acid is synthesized from mevalonic acid in living cells. It is possible that under certain circumstances, abscisic acid or closely related compounds are formed by the oxidation of carotenoids.16The sites of gibberellin production are sites of cell death. It is possible that precursors of gibberellins, such as kaurene, are oxidized to gibberellins when cells die.17Cytokinins are present in transfer‐RNA (tRNA) of animals, fungi, bacteria and higher plants. They are probably formed in plants by the hydrolysis of tRNA in autolysing cells. There is evidence that they are also formed in living cells in root tips.18Ethylene is produced in senescent, dying or damaged cells by the breakdown of methionine.19It was shown many years ago that wounded and damaged cells produced sub stances which stimulate cell division. It now seems likely that the production of wound hormones and the normal production of hormones as a consequence of cell death are two aspects of the same phenomenon. Wounded cells can produce auxin, gibberellins, cytokinins and ethylene.20The control of hormone production in living cells is a biochemical problem which remains unsolved. The control of production of hormones formed as a con sequence of cell death depends on the control of cell death itself. Cell death is con trolled by hormones which are themselves produced as a consequence of cell death.21In spite of the fact that dying cells are present in all vascular plants, in all wounded and infected tissues, in certain differentiating tissues in animals, in cancerous tumours and in developing animal embryos, the biochemistry of cell death is a subject which has been almost completely ignored. Dying cells are an important source of hormones in plants; some of the many substances released by dying cells may also be of physiologica

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1973.tb01568.x

出版商:Blackwell Publishing Ltd    

年代:1973

数据来源: WILEY

摘要:

SUMMARY1A samara is a winged fruit or seed that autorotates when falling, thereby reducing the sinking speed of the diaspore and increasing the distance it may be transported by winds. Samaras have evolved independently in a large number of plants.2Aerodynamical, mechanical, and structural properties crucial for the inherent self‐stability are analysed, and formulae for calculation of performance data are given.3The momentum theorem is applied to samaras to calculate induced air velocities. As a basis for blade element analysis, and for directional stability analysis, various velocity components are put together into resultant relative air velocities normal to the blade's span axis for a samara in vertical autorotation and also in autorotation with side‐slip.4When falling, a samara is free to move in any sense, but in autorotation it possesses static and dynamic stability. Mainly qualitative aspects on static stability are pre sented. Simple experiments on flat plates at Reynolds numbers about 2000 as in samaras, showed that pitch stability prevails when the C. M. (centre of mass) is located 27–35 % of the chord behind the leading edge. The aerodynamic c.p. (centre of pressure) moves forward upon a decrease of the angle of attack, backward upon an increase. In samara blades the c.m. liesca. one‐third chord behind the leading edge, and hence the aerodynamic and centrifugal forces interact so as to give pitch stability, involving stability of the angles of attack and gliding angles.5Photographs show that the centre of rotation of the samara approximately coincides with its c.m.6The coning angle (blade angle to tip path plane) taken up by the samara is determined by opposing moments set up by the centrifugal and aerodynamic forces. It is essentially the centrifugal moment (being a tangent function of the coning angle, which is small) that changes upon a change of coning angle, until the centrifugal and aerodynamic moments cancel out at the equilibrium coning angle.7Directional stability is maintained by keeping the tip path plane horizontal whereby a vertical descent path relative to the ambient air is maintained. Tilting of the tip path plane results in side‐slip. Side‐slip leads to an increased relative air speed at the blade when advancing, a reduced speed when retreating. The correspondingly fluctuating aerodynamic force and the gyroscopic action of the samara lead to restoring moments that bring the tip path plane back to the horizontal.8Entrance into autorotation is due to interaction between aerodynamic forces, the force of gravity, and inertial forces (when the blade accelerates towards a trailing position behind the c.m. of the samara).9The mass distribution must be such that the c.m. lies 0–30 % of the span from one end. InAcerandPlceasamaras the C.M. lies 10–20% from one end, thereby making the disk area swept by the blade large and the sinking speed low.10The blade plan‐form is discussed in relation to aerodynamics. The width is largest far out on the blade where the relative air velocities are large. The large width of the blade contributes to a highRenumber and thus probably to a betterL/D(lift/drag) ratio and a slower descent.11The concentration of vascular bundles at the leading edge of the blade and the tapering of the blade thickness towards the trailing edge are essential for a proper chord wise mass distribution.12Data are given for samaras ofAcerandPlcea, and calculations of performance are made by means of the formulae given in the paper. Some figures for anAcersamara are: sinking speed 0.9 m/sec, tip path inclination 15°, average total force coefficient 1.7 (which is discussed), and aL/Dratio of the blade approximately 3.13The performances of samaras are compared with those of insects, birds, bats, a flat plate, and a parachute. They show the samara to be a relatively very efficient structure in braking the sinking speed of the diaspore.14In samaras the mass, aerodynamic, and torsion axes coincide, whereas in insect wings the torsicn axis often lies ahead of the other two. Location of the torsion axis in front of the aerodynamic axis in insects tends towards passive wing twisting and passive adjustment of the angles of attack relative to the incident air stream, the direction of which varies along the wing because of wing flapping.15Location of the mass axis behind the torsion axis may l

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1973.tb01569.x

出版商:Blackwell Publishing Ltd    

年代:1973

数据来源: WILEY

摘要:

SUMMARY1The view is supported that chitin is not found in Deuterostomia because of the absence of chitin synthetase, and is not found in higher plants because of the absence of glucosamine. In Fungi, control mechanisms are present affecting the synthesis of glucosamine; chitin is often present, but when it is absent this probably results from a failure to synthesize glucosamine.2A review of conformation maps for cellulose and chitin indicates the possibility of a slightly right‐handed twist in small groups of chitin chains.3The occurrence of α, β and γ‐forms of chitin in the peritrophic membranes of various insects is described. Gamma chitin seems to be the commonest form.4In several beetles, optical and electron‐microscope studies trace the formation of chitinous cocoon fibres from larval peritrophic membrane and define the discrete ribbon‐like nature of the,βchitin produced in the mid‐gut.5By studying apodemes it is found that orthopteroid insects are most varied, different molecular structures being present in levator, depressor and pretarsal tendons. By contrast, Hymenoptera and Coleoptera show very similar structures in all three apodemes as well as in other parts of the cuticle. Apodemes are regarded as sampling the cuticle at their varying points of origin; they provide especially favour able material for diffraction studies.6In arthropod cuticles there is evidence for the widespread occurrence of α chitin micelles which are three chains thick in the direction of thecaxis. This is compared with the structure of γ chitin where the chains repeat in groups of three along thecaxis.7Changes in the diffraction pattern are related to the series of proteins defined by Hackman. The chitin‐protein complex is not affected by water or neutral salt extrac tion, but is disrupted by treatment in urea.8Electron microscopy defines the unit of structure as a composite microfibril: a core of chitin surrounded by adsorbed proteins. This consists of ‘primary’ protein (often repeating as regular units along the fibrils) and a quantity of ‘satellite’ protein which obscures the imaging of the regularly arranged ‘primary’ protein. There are apparent ‘bridges' between the microfibrils.9New diffraction data give information about the size and arrangement of micro‐fibrils. These fibrils may be arranged in layers of ‘rods’, or a

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1973.tb01570.x

出版商:Blackwell Publishing Ltd    

年代:1973

数据来源: WILEY

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1973.tb01571.x

出版商:Blackwell Publishing Ltd    

年代:1973

数据来源: WILEY