The Rest Period of Rhododendron Flower Buds: III. CYTOLOGICAL STUDIES ON THE ACCUMULATION AND BREAKDOWN OF PROTEIN BODIES AND AMYLOPLASTS DURING FLOWER DEVELOPMENT

Rhododendron flower development occurs in three easily definedstages: a pre-rest stage, during which petal growth is mainlyby cell elongation; an indeterminate rest period; and an after-reststage, that begins when the flowers resume growth and ends atanthesis. Early in the pre-rest stage of development, protein bodies andamyloplasts accumulate in the petals. The epidermal cells accumulateonly protein bodies and the mesophyll cells accumulate amyloplaststhat have a few small protein bodies around the periphery. Thesubepidermal cells and the cells around the vascular bundlesaccumulate both large protein bodies and amyloplasts. Duringthe rest period there is a cessation of cell elongation andthe reserve protein bodies and amyloplasts remain intact. The protein bodies in all of the cells including those aroundthe amyloplasts are proteolized early in the after-rest stageof development. Digestion of the starch granules occurs whenthe petals are about one-half their final size. Epidermal-cell expansion during after-rest is relatively uniform;the walls between adjacent epidermal cells remain attached toeach other. The mesophyll cells elongate irregularly and thewalls of adjacent cells separate giving rise to large intercellularspaces. At anthesis the petal cells consist of a cell wall, a parietalcytoplasm, and a large central vacuole.     

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.