Changes In Tail Length Research Articles

Evolution of the structure of tail feathers: implications for the theory of sexual selection.

Bird tails are extraordinarily variable in length and functionality. In some species, males have evolved exaggeratedly long tails as a result of sexual selection. Changes in tail length should be associated with changes in feather structure. The study of the evolution of feather structure in bird tails could give insight to understand the causes and means of evolution in relation to processes of sexual selection. In theory, three possible means of tail length evolution in relation to structural components might be expected: (1) a positive relationship between the increase in length and size of structural components maintaining the mechanical properties of the feather; (2) no relationship; that is, enlarging feather length without changes in the structural components; and (3) a negative relationship; that is, enlarging feather length by reducing structural components. These hypotheses were tested using phylogenetic analyses to examine changes in both degree of exaggeration in tail length and structural characteristics of tail feathers (rachis width and density of barbs) in 36 species, including those dimorphic and nondimorphic in tail length. The degree of sexual dimorphism in tail length was negatively correlated with both rachis width and density of barbs in males but not in females. Reinforcing this result, we found that dimorphism in tail length was negatively associated with dimorphism in tail feather structure (rachis width and density of barbs). These results support the third hypothesis, in which the evolution of long feathers occurs at the expense of making them simpler and therefore less costly to produce. However, we do not know the effects of enfeeblement on the costs of bearing. If the total costs increased, the enfeeblement of feathers could be explained as a reinforcement of the honesty of the signal. Alternatively, if total costs were reduced, the strategy could be explained by cheating processes. The study of female preferences for fragile tail feathers is essential to test these two hypotheses. Preferences for fragile tails would support the evolution of reinforcement of honesty, whereas female indifference would indicate the existence of cheating in certain stages of the evolutionary process.

EVOLUTION OF THE STRUCTURE OF TAIL FEATHERS: IMPLICATIONS FOR THE THEORY OF SEXUAL SELECTION

Bird tails are extraordinarily variable in length and functionality. In some species, males have evolved exaggeratedly long tails as a result of sexual selection. Changes in tail length should be associated with changes in feather structure. The study of the evolution of feather structure in bird tails could give insight to understand the causes and means of evolution in relation to processes of sexual selection. In theory, three possible means of tail length evolution in relation to structural components might be expected: (1) a positive relationship between the increase in length and size of structural components maintaining the mechanical properties of the feather; (2) no relationship; that is, enlarging feather length without changes in the structural components; and (3) a negative relationship; that is, enlarging feather length by reducing structural components. These hypotheses were tested using phylogenetic analyses to examine changes in both degree of exaggeration in tail length and structural characteristics of tail feathers (rachis width and density of barbs) in 36 species, including those dimorphic and nondimorphic in tail length. The degree of sexual dimorphism in tail length was negatively correlated with both rachis width and density of barbs in males but not in females. Reinforcing this result, we found that dimorphism in tail length was negatively associated with dimorphism in tail feather structure (rachis width and density of barbs). These results support the third hypothesis, in which the evolution of long feathers occurs at the expense of making them simpler and therefore less costly to produce. However, we do not know the effects of enfeeblement on the costs of bearing. If the total costs increased, the enfeeblement of feathers could be explained as a reinforcement of the honesty of the signal. Alternatively, if total costs were reduced, the strategy could be explained by cheating processes. The study of female preferences for fragile tail feathers is essential to test these two hypotheses. Preferences for fragile tails would support the evolution of reinforcement of honesty, whereas female indifference would indicate the existence of cheating in certain stages of the evolutionary process.

The casein mRNA decay changes in parallel with the poly(A) tail length in the mouse mammary gland

Using β- and γ-casein mRNAs, the relationship between poly(A) tail length and half-life of mRNA is determined in the mouse mammary gland during pregnancy and lactation. β- and γ-Casein mRNAs increase before and after parturition, respectively. The poly(A) tail as well as the half-life of casein mRNA becomes longer upon the active casein mRNA synthesis. The poly(A) tail is shortened gradually as lactation progresses. The half-life of mRNA decreases approximately from 20 h at early to 4 h at late lactation. Northern blot analysis reveals that nuclear RNA has the same poly(A) tail length as casein mRNA in the cytoplasm does. Thus, the mammary gland changes the poly(A) tail length of casein mRNA. The poly(A) tail length changes in parallel with the level of poly(A) polymerase (PAP) mRNA during pregnancy and lactation, suggesting that the mammary gland determines the poly(A) tail length of casein mRNA through the change in the PAP gene expression. As the half-life of casein mRNA is related with the degree of polyadenylation, we conclude that the poly(A) tail elongation and shortening is a mechanism in regulating the mRNA decay.

Systemic treatment with epidermal growth factor causes organ growth concomitant with reduced circulating levels of IGF-I and IGFBP-3: time-dependent changes in female rats

Systemic treatment with epidermal growth factor (EGF) in neonatal rats reduces circulating levels of insulin-like growth factor I (IGF-I) and causes somatic growth retardation. In this study, we investigated the effects of EGF treatment on the IGF system and on visceral organ growth and longitudinal growth in mature rats. We treated female Wistar rats for 0 (n = 16), 1 (n = 8), 2 (n = 8), 3 (n = 8), or 4 (n = 8) weeks with subcutaneous EGF (150 microg/kg/day). The animals were weighed once a week. At sacrifice, various viscera were removed and weighed. Blood and serum samples obtained at sacrifice were analysed for growth hormone (GH), IGF-I, IGF binding proteins (IGFBPs) and various routine parameters. EGF treatment increased the total body weight. All parts of the gastrointestinal tract, the liver, the pancreas, the spleen, the bladder, the suprarenal glands and the ovaries increased proportionately more in weight than the increase in total body weight; the heart and the kidneys increased proportionately in weight whereas the weight of the perirenal fat was reduced. There were no changes in tail length but the mean length of the tibia was slightly increased in the group treated for 4 weeks with EGF. Circulating GH was unchanged but IGF-I and IGFBP-3 were reduced approximately 25 and 45%, respectively, in all EGF treated groups. There were no changes in the hepatic content of IGF-I and IGFBPs. In conclusion, systemic EGF treatment causes visceral growth concomitant with reduced circulating levels of IGF-I and IGFBP-3 in mature female rats.

SEXUAL SELECTION IN THE MONOGAMOUS BARN SWALLOW (HIRUNDO RUSTICA). I. DETERMINANTS OF TAIL ORNAMENT SIZE.

The proportion of phenotypic variance in the length of the sexually selected tail of the monogamous barn swallow Hirundo rustica that is attributable to genetic variance was studied in the field in Denmark during a seven-year period. Tail length was on average 20% greater in males than in females. Tail length correlated with wing length, but not with other morphological traits. Tail length increased with the first molt, but remained constant during subsequent years. Changes in tail length between years, owing to molt were significantly affected by sex and by degree of infection with an haematophagous mite (Ornithonyssus bursa). There were significant differences in sexual size dimorphism between years, apparently as a result of environmental conditions in the African winter quarters during molt. Tail length was a highly repeatable morphological trait, and standardization of tail length for age effects only marginally increased repeatability. Heritability of tail length as estimated from regression of values for sons on those of their fathers was 0.59. This suggests that secondary sexual traits affected by strong directional selection still may show a statistically significant heritability.

Catch-up growth in cortisone-treated rats: effects of calcium and vitamin D.

Summary: The aim of the study was to develop an animal model of steroid stunting and catch-up growth and to investigate the possibility that calcium supplements, with or without vitamin D supplements, might mitigate the effects of corticosteroids on linear growth. In the first experiment, newly weaned Wistar rats were allocated to four groups and weight and tail length measured weekly. In three groups cortisone was injected daily for 28 days. Two of the cortisone-treated groups were given calcium supplements daily in different dosage schedules. During cortisone treatment (Table 1), animals given cortisone gained less weight than the controls (P <0.01). After cortisone was stopped the groups previously given cortisone showed greater weight gain than the controls (P <0.01). Changes in tail length (Fig. 2), representing changes in linear growth, showed that groups receiving cortisone grew less than the controls during cortisone treatment. After cortisone was stopped the control group grew less than the three groups that had previously received cortisone. There was no beneficial effect of supplemental calcium on either the degree of growth retardation or of catch-up growth (Tables 1 and 2). A second experiment was performed to test the reproducibility of the method and to study the effects of calcium and vitamin D supplements on growth. Newly weaned rats were allocated to four groups. Three groups received cortisone for 42 days. Two of the cortisone-treated groups received vitamin D once a week and one of these groups received calcium supplements. Weight and tail length velocities (Figs. 5 and 6) show less velocity than that of the cortisone-treated groups during cortisone treatment, and after cortisone was stopped the control group had lesser velocity. During cortisone treatment (Table 3), the control groups gained more weight than the three groups given cortisone (P <0.001). After cortisone was stopped the groups previously receiving cortisone gained more weight than the control group (P <0.01 for cortisone alone and P <0.001 for cortisone and vitamin D). Changes in mean tail lengths (Table 4) show that during cortisone treatment the three groups given cortisone alone, cortisone and vitamin D, and cortisone, vitamin D, and calcium, all gained less than the controls (P <0.001). After cortisone was stopped the groups previously treated with cortisone had a greater increase in tail length than the control groups (P <0.001). The group given vitamin D supplements grew more than the group given cortisone without such supplements (P <0.01). The food consumed by the animals (g/100 g body wt/day) was measured (Fig. 7), and at no time did the control group eat more than the cortisone-treated groups. Reduced calorie intake was not the explanation for retardation of growth, and the increased food intake after cortisone was presumably necessary for catch-up. The serum calcium and total body calcium at the end of the experiment (Table 5) did not suggest that cortisone had depleted the skeleton of calcium. The experiment confirmed that cortisone inhibits growth of total body weight and of tail length in newly weaned rats, but the total growth of all groups was similar by the end of the experiment and confirmed that catch-up growth had occurred. The groups given vitamin D supplements had a greater increase in tail length in the catch-up phase than the group given cortisone without such supplements. It may be that vitamin D had a specific effect on the growth plate, ameliorating the effects of corticosteroids on growing cartilage. Speculation: The growth retardation induced by cortisone may be partly related to direct effects on the skeleton. Vitamin D may improve catch-up growth by antagonizing the effects of corticosteroids on the growth plate.