Competitive behaviour and feeding rate in a reintroduced population of Griffon Vultures Gyps fulvus

Intraspecific competitive behaviours were studied in a reintroduced population of Griffon Vultures Gyps fulvus in order to describe the pattern of competition between ages and sexes, assess the effect of reintroduction on competitive behaviour, and study the potential consequences of food management on competition. There was no evidence for a difference in feeding or display rates between age classes. However interaction rates, aggressiveness and dominance were higher in old adults than in the other age classes. No difference in the pattern of competition was found between sexes. There was no difference in the competitive ability (feeding rate and dominance) of reintroduced and wild-bred individuals. Feeding rates increased with resource availability. Group size also increased with food mass, but was lower than the theoretical maximum number of birds. This may be evidence of competition by interference where some individuals are able to increase their feeding rate by the exclusion of others. An increase in both the number of carcasses and the number of feeding sites is thus recommended to induce dispersal and reduce this competition.     

Effect of the 1990 die-off in the northern Italian seas on the developmental stability of the striped dolphin Stenella coeruleoalba (Meyen, 1833)

Developmental stability of the community of striped dolphins, Stenella coeruleoalba (Meyen, 1833), that died during the Mediterranean epizootic of 1990 was compared with that of the population prior to and after the epizootic, to assess whether animals that died were the developmentally less stable individuals in the population. Significantly higher levels of fluctuating asymmetry (FA) were found in those individuals that died. Tissue levels of organochlorine pesticide residues and PCBs were determined and the correlation between contaminant concentration and FA was tested. No correlations were found between the contaminant level and FA.     

A Maize Mutant with an Altered Vascular Pattern

A recessive maize mutant with disrupted seedling developmentwas isolated following transpositional mutagenesis with Mutator.This mutant, initially identified during germination on thebasis of abnormal growth of the scutellar node, was designatedlsn1 (l arge s cutellar n ode). The mutant seedling exhibitsan enlarged primary root with a longitudinal groove and multipleseparate root tips. The mutant root is shorter than normal,because of defective cell elongation, and lacks lateral roots.The mutant plant shows defective leaves and reduced internodeelongation. Histological analyses on primary root, shoot, scutellarnode and juvenile leaves revealed a series of defects, all relatedto an irregular differentiation of vascular elements. In addition,in situ hybridization of mutant leaves demonstrates an abnormalpattern of expression of Knotted-1, a marker of meristem function.The presence of multiple roots fused together can be interpretedas suppression of the negative control responsible for the differentiationof only one root primordium. Therefore, the data obtained onseedlings of lsn1 point to a relationship between meristem activity,vascular differentiation and auxin polar transport, and mayallow the identification of a gene which is active during embryogenesis.Copyright2000 Annals of Botany Company Auxin, defective seedling, maize, meristem activity, vascular differentiation, Zea mays.     

NO signalling in cytokinin-induced programmed cell death

Cell death can be induced by cytokinin 6-benzylaminopurine (BA) at high dosage in suspension-cultured Arabidopsis cells. Herein, we provide evidence that BA induces nitric oxide (NO) synthesis in a dose-dependent manner. A reduction in cell death can be observed when the cytokinin is supplemented with the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) or the nitric oxide synthase (NOS) inhibitors: 2-aminoethyl-isothiourea (AET) and N^G.-monomethyl- l -arginine ( l -NMMA), which suggests that NO is produced via a NOS and is a signalling component of this form of programmed cell death. In BA-treated cells, mitochondrial functionality is altered via inhibition of respiration. This inhibition can be prevented by addition of either cPTIO or AET implying that NO acts at the mitochondrial level.