Embryonic temperature determines adult sexuality in a reptile

Gonadal differentiation in amniote vertebrates is controlled by one of two mechanisms: genotypic sex determination (GSD) or environmental sex determination (ESD). After differentiation the fetal gonad produces sex steroid hormones which govern the development of other components of sexuality. Thus, the primary sex determiner is thought to operate solely as a trigger that initiates a cascade of events culminating in adult sex differences. In the leopard gecko (Eublepharis macularius), gonadal and morphological sex is determined by incubation temperature, with relatively 'hot' temperatures (32 degrees C) resulting in mostly male offspring and relatively 'cold' temperatures (26 degrees C) resulting in only female offspring. We report here that the reproductive behaviour and endocrine physiology of an adult is influenced by the temperature experienced as an embryo. Also, the perception of a female to courtship by a male is influenced by incubation temperature. These data indicate that incubation temperature, the primary determiner of sex in this species, has differential effects on adult sexuality.     

Nucleotide sequence of a region of human mitochondrial DNA containing the precisely identified origin of replication

A fragment of HeLa cell mitochondrial DNA containing the origin of replicaton has been sequenced. The precise position of the origin in this sequence has been identified by determining the nucleotide order in the 5'-end proximal portion of the heavy strand initiation fragment (7S DNA), and by aligning the two sequences.     

Acceleration of beta-receptor desensitization in combined administration of antidepressants and phenoxybenzamine

The delayed therapeutic effects of antidepressants (usually between 10 and 14 days) and of the tricyclic antidepressants in particular, are believed (on the basis of animal experiments) to lie in a progressive decrease of the sensitivity of cortical beta-adrenergic receptors. This is thought to be due to an increase in the synaptic concentration of noradrenaline, in turn accomplished by a decrease in the sensitivity of the presynaptic alpha 2 receptors which normally regulate noradrenaline secretion by a negative feedback mechanism. This model suggests that the desensitization of postsynaptic beta-receptors by antidepressants should be accelerated by the inhibition of the presynaptic alpha 2- adrenergic system, and we have indeed observed such an effect in preliminary studies with desipramine and phenoxybenzamine (PBZ) combined. We now show that the administration of either tricyclic or monoamine oxidase inhibitor antidepressants in combination with PBZ, an irreversible alpha-adrenergic blocker, accelerates and intensifies the desensitization of beta-adrenergic receptors. Our observations may have therapeutic implications.