Heterogeneous binding of high mobility group chromosomal proteins to nuclei

A dramatic difference is observed in the intracellular distribution of the high mobility group (HMG) proteins when chicken embryo fibroblasts are fractionated into nucleus and cytoplasm by either mass enucleation of cytochalasin-B-treated cells or by differential centrifugation of mechanically disrupted cells. Nuclei (karyoplasts) obtained by cytochalasin B treatment of cells contain more than 90 percent of the HMG 1, while enucleated cytoplasts contain the remainder. A similar distribution between karyoplasts and cytoplasts is observed for the H1 histones and the nucleosomal core histones as anticipated. The presence of these proteins, in low amounts, in the cytoplast preparation can be accounted for by the small percentage of unenucleated cells present. In contrast, the nuclei isolated from mechanically disrupted cells contain only 30-40 percent of the total HMGs 1 and 2, the remainder being recovered in the cytosol fraction. No histone is observed in the cytosol fraction. Unike the higher molecular weight HMGs, most of the HMGs 14 and 17 sediment with the nuclei after cell lysis by mechanical disruption. The distribution of HMGs is unaffected by incubating cells with cytochalasin B and mechanically fractionating rather than enucleating them. Therefore, the dramatic difference in HMG 1 distribution observed using the two fractionation techniques cannot be explained by a cytochalasin-B-induced redistribution. On reextraction and sedimentation of isolated nuclei obtained by mechanical cell disruption, only 8 percent of the HMG 1 is released to the supernate. Thus, the majority of the HMG 1 originally isolated with these nuclei, representing 35 percent of the total HMG 1, is stably bound, as is all the HMGs 14 and 17. The remaining 65 percent of the HMGs 1 and 2 is unstably bound and leaks to the cytosol fraction under the conditions of mechanical disruption. It is suggested that the unstably bound HMGs form a protein pool capable of equilibrating between cytoplasm and stably bound HMGs.     

Hormonal factors controlling the initiation and development of lateral roots

The decapitated primary root of 3-day-old Alaska pea seedlings has been used as a test system to determine the activities on lateral root formation of six auxins, six cytokinins and several other naturally-occurring compounds. Their effects were assessed on (1) the initiation of lateral root primordia, (2) the emergence of visible lateral roots, and (3) the elongation of these laterals. All the auxins, at the optimum concentration of 10^-4M, promoted the initiation of lateral root primordia, and all except 3-indolylpropionic acid inhibited the elongation of the resulting lateral roots. Their effects on the emergence of laterals were small and varied. All the cytokinins, at 10^-6M and above, inhibited both the initiation and the emergence of lateral roots, zeatin being the most powerful inhibitor. The emergence process was about twice as sensitive as the initiation of primordia to the presence of cytokinins. The cytokinin ribosides were generally less active than the free bases. Abscisic acid and xanthoxin inhibited both emergence and elongation, the concentration for 50% decrease of emergence being about 10^-4M. Gibberellic acid had little clear effect on any of the three criteria. Nicotinic acid and thiamine at 10^-3M promoted both the initiation of primordia and their emergence: pyridoxal phosphate stimulated both emergence and elongation but did not influence the initiation of primordia. Adenine and guanine had little effect but decreased root elongation some 25%. The strong inhibiting effect of the cytokinins may well be the basis for the marked inhibition exerted by the root-tip on lateral root formation, while the promoting effects of auxins may explain the previously observed promotion of lateral root formation by the young shoot and cotyledons.     

Nociceptive Response to Prostaglandins and Analgesic Actions of Aspirin and Morphine

VANE et al.^1–3 have proposed that aspirin and allied antiinflammatory drugs act by inhibiting the production of prostaglandins in the tissues. Because, however, prostaglandins E₁ and E₂ (PGE₁ and PGE₂) had been reported not to elicit pain in human skin at doses inducing inflammation^{4, 5}, Vane did not suggest that the inhibition of prostaglandin production fully explains the analgesic action of aspirin-like drugs. Nonetheless, PGE₁ PGE₂ or PGF_2α irritates pulmonary^{6, 7} or ocular⁸ mucous membrane and, when injected by the subcutaneous or intramuscular route, PGE₂ or PGF_2α causes pain⁹.     

Molecular evolution of rodent insulins

Several trees of amino acid sequences of rodent insulins were derived with the maximum-parsimony procedure. Possible orthologous and paralogous relationships were investigated. Except for a recent gene duplication in the ancestor of rat and mouse, there are no strong arguments for other paralogous relationships. Therefore, a tree in agreement with other biological data is the most reasonable one. According to this tree, the capacity to form zinc-binding hexamers was lost once in the ancestor of the hystricomorph rodents, followed by moderately increased evolutionary rates in the lineages to African porcupine and chinchilla but highly increased rates in at least three independent lines to other taxa of this suborder: guinea pig, cuis, and Octodontoidea (coypu and casiragua).