In Arabidopsis thaliana, FRD3 (FERRIC CHELATE REDUCTASE DEFECTIVE 3) plays a central role in metal homeostasis. FRD3 is among a set of metal homeostasis genes that are constitutively highly expressed in roots and shoots of Arabidopsis halleri, a zinc hyperaccumulating and hypertolerant species. Here, we examined the regulation of FRD3 by zinc in both species to shed light on the evolutionary processes underlying the evolution of hyperaccumulation in A. halleri. We combined gene expression studies with the use of β-glucuronidase and green fluorescent protein reporter constructs to compare the expression profile and transcriptional and post-transcriptional regulation of FRD3 in both species. The AtFRD3 and AhFRD3 genes displayed a conserved expression profile. In A. thaliana, alternative transcription initiation sites from two promoters determined transcript variants that were differentially regulated by zinc supply in roots and shoots to favour the most highly translated variant under zinc-excess conditions. In A. halleri, a single transcript variant with higher transcript stability and enhanced translation has been maintained. The FRD3 gene thus undergoes complex transcriptional and post-transcriptional regulation in Arabidopsis relatives. Our study reveals that a diverse set of mechanisms underlie increased gene dosage in the A. halleri lineage and illustrates how an environmental challenge can alter gene regulation.
In order to study in vitro chemotaxis, phagocytosis and bactericydal efficiencies of granulocytes (PMN) and monocytes (Mo) of cancer patients with solid tumours, the authors have undertaken the evaluation of a method of measuring PMN and Mo chemotaxis with modified Boyden chambers, using In-111-oxine. The tests were performed in order to evaluate the interference of N-etilmycin with leukocyte functions, a currently fashionable antibiotic used in the treatment of gram-negative infections. The results both compare well with the visual method and are objective. Cancer patients, disease-free for a minimum of one year, were compared and evidenced normal chemotaxis and normal controls. No difference between the two groups was found (20.46% of those tested). The addition of N-etilmy-cin (6..mu..g/ml) to PMN and Mo further decreased the chemotaxis from 20.46% to 16.07% (t=2.81, P=0.0102). The addition of 30..mu..g/ml further decreased the chemotaxis from the mean control values to 5.925% (t=4.55,P 1%). The use of N-etilmycin in disease-free cancer patients should be avoided in the possible event of tumour enhancement.
Les telomeres Chez l’homme, les telomeres sont des sequences repetees d’ADN (5’-TTAGGG-3’) presentes a l’extremite des chromosomes. Ces telomeres sont couverts d’un complexe de proteines (shelterin complex) qui assure une protection des terminaisons chromosomiques et evite que l’extremite du chromosome ne soit consideree comme une rupture du double brin d’ADN ; ceci pourrait en effet conduire a des soudures de chromosomes par fusion de leurs telomeres respectifs et une perte de l’integrite du materiel genetique [1] (Figure 1a). A chaque duplication d’un chromosome lors de la division cellulaire, l’ADN polymerase est incapable de recopier completement l’extremite des telomeres. Ces telomeres raccourcissent donc progressivement et, lorsque leur taille devient critique, la cellule stoppe irreversiblement sa croissance. On dit que la cellule entre en senescence : elle « vieillit ». Les telomeres constituent donc des « horloges biologiques » [2]. Pour proliferer indefiniment et dejouer la barriere imposee par le raccourcissement des telomeres, la plupart des cellules cancereuses expriment une enzyme, baptisee telomerase, dont l’activite permet de recopier les extremites telomeriques, permettant ainsi de maintenir la longueur des telomeres constante au cours des divisions cellulaires [2, 11, 12].
