Allometric cascade as a unifying principle of body mass effects on metabolism

The power function of basal metabolic rate scaling is expressed as aM(b), where a corresponds to a scaling constant (intercept), M is body mass, and b is the scaling exponent. The 3/4 power law (the best-fit b value for mammals) was developed from Kleiber's original analysis and, since then, most workers have searched for a single cause to explain the observed allometry. Here we present a multiple-causes model of allometry, where the exponent b is the sum of the influences of multiple contributors to metabolism and control. The relative strength of each contributor, with its own characteristic exponent value, is determined by the control contribution. To illustrate its use, we apply this model to maximum versus basal metabolic rates to explain the differing scaling behaviour of these two biological states in mammals. The main difference in scaling is that, for the basal metabolic rate, the O(2) delivery steps contribute almost nothing to the global b scaling exponent, whereas for the maximum metabolic rate, the O(2) delivery steps significantly increase the global b value.     

A histochemical study of the pectoralis muscle of the south indian flying lizard,Draco dussumieri

Résumé Le muscle pectoral duDraco dussumieri comprend des fibres de trois sortes: minces, intermédiaires et épaisses. Les fibres minces sont adaptées à un métabolisme glycolytique et les fibres épaisses au lipolytique. L'activité des fibres minces révèle la présence de phosphorylase et de synthétase glycogénique.     

DNA sequence organisation in relation to genome size in birds

Summary DNA sequence interspersion was investigated in pheasant and pelican nuclear DNA. As is typical for birds, these genomes are organized in a long period pattern. Altogether, 5 bird species with genome sizes between 1.6 and 1.9 pg DNA are compared with regard to the extent of repetitive and single copy sequence interspersion. The result indicates that the average length of interspersed repetitive sequences increases with genome size.Acknowledgment. This work was supported by the Deutsche Forschungsgemeinschaft. Mrs H. Tuczynski and Mr J. S. Jackson are thanked for editorial assistance.     

Essential role for Nix in autophagic maturation of erythroid cells

Erythroid cells undergo enucleation and the removal of organelles during terminal differentiation. Although autophagy has been suggested to mediate the elimination of organelles for erythroid maturation, the molecular mechanisms underlying this process remain undefined. Here we report a role for a Bcl-2 family member, Nix (also called Bnip3L), in the regulation of erythroid maturation through mitochondrial autophagy. Nix(-/-) mice developed anaemia with reduced mature erythrocytes and compensatory expansion of erythroid precursors. Erythrocytes in the peripheral blood of Nix(-/-) mice exhibited mitochondrial retention and reduced lifespan in vivo. Although the clearance of ribosomes proceeded normally in the absence of Nix, the entry of mitochondria into autophagosomes for clearance was defective. Deficiency in Nix inhibited the loss of mitochondrial membrane potential (DeltaPsi(m)), and treatment with uncoupling chemicals or a BH3 mimetic induced the loss of DeltaPsi(m) and restored the sequestration of mitochondria into autophagosomes in Nix(-/-) erythroid cells. These results suggest that Nix-dependent loss of DeltaPsi(m) is important for targeting the mitochondria into autophagosomes for clearance during erythroid maturation, and interference with this function impairs erythroid maturation and results in anaemia. Our study may also provide insights into molecular mechanisms underlying mitochondrial quality control involving mitochondrial autophagy.