On the failure of two butterfly species to respond to the presence of conspecific eggs prior to oviposition

Abstract. 1. The eggs of Euptychiine butterflies are laid singly, but their distributions tend to be contagious. However, these insects do not discriminate between egg-laden and egg-free plants.
2. Response to conspecific eggs is not part of the mechanism responsible for clumped egg distribution.     

Inactivation of Calcitonin by Specific Organs

THE greater biological potency of salmon calcitonin (SCT) as compared with mammalian calcitonins may be due to the relative resistance of SCT to inactivation in vivo^1,2. SCT infused into dogs disappears from the circulation more slowly than does porcine calcitonin (PCT) or human calcitonin (HCT)^1–3. For example, the metabolic clearance rate (MCR) of PCT in the dog is approximately 10 times greater than that of SCT^1,2. Neither renal excretion^3,4 nor inactivation by plasma^1,2 is sufficient to account for the rapid clearance of the calcitonins that we have observed in vivo and thus it seemed likely that inactivation of the hormones must occur during passage through one or more organs. Here we present data that suggest the kidney, the liver and muscle and/or bone as the sites of inactivation of the calcitonins in the dog. SCT is relatively resistant to inactivation in the latter two sites.     

Mutant tRNA<Superscript>His</Superscript> Ineffective in Repression and Lacking Two Pseudouridine Modifications

TRANSFER RNA has been implicated in the regulation of a number of amino-acid biosynthetic operons^1–4. Histidyl-tRNA^His has been shown to be involved in regulation of the histidine operon by analysis of six genes (hisO, hisR, hisS, hisT, hisU, hisW), mutation of which causes derepression of the enzymes of the histidine biosynthetic pathway in Salmonella typhimurium^5–7. A class of derepressed mutants (hisR) has only about 55% as much tRNA^His as the wild type⁴ and in the one example sequenced, contains tRNA^HIS with a structure identical to that of the wild type⁸. Studies of mutants of the gene for histidyl-tRNA synthetase (hisS) indicated that the derepressed phenotype was associated with defects in the charging of tRNA^HISin vitro². The amounts of charged and uncharged tRNA^His present in vivo during physiological derepression of the wild type and in the six classes of regulatory mutants, have been determined⁹. This work has shown that repression of the histidine operon is correlated directly with the concentration of charged histidyl-tRNA^Hisin vivo and not with the ratio of charged to uncharged or the absolute amount of uncharged tRNA^His. The derepression observed in mutants, of hisS (the gene for histidyl-tRNA synthetase), hisR (the presumed structural gene for the single species of tRNA^His) and hisU and hisW (genes presumably involved in tRNA modification) may be explained by the lower cellular concentration of charged tRNA^His which these mutants contain.