Cytoskeleton and PCH-induced pigment aggregation in Macrobrachium potiuna erythrophores.
Herein we report the effects of microtubule- and actin-like filament disrupting drugs, as well as the microtubule stabilizer taxol, on PCH-induced pigment granule aggregation within erythrophores of the freshwater crustacean Macrobrachium potiuna. Dose-response curves (DRCs) to the pigment-concentrating hormone PCH were determined under control and experimental conditions to evaluate the effects elicited by the cytoskeleton-affecting drugs. Colchicine, at temperatures 22 degrees C and 4 degrees C, and vinblastine significantly inhibited the aggregating response to PCH and affected the dynamics of the process, as shown by the change in the slope of the regression curve calculated from the DRCs. Lumicolchicine, a colchicine analogue with no affinity for tubulin, also inhibited pigment migration, though no change in the slope of the regression curve was observed. The inhibitory effects of lumicolchicine demonstrate that changes in sites other than cytoskeleton, such as membrane permeability, may also cause a decrease in the PCH-induced aggregating responses and that the colchicine effects may result from its action on cellular sites additional to the cytoskeleton. Taxol, a microtubule stabilizer, did not affect the DRC to PCH, and DMSO improved the PCH-evoked responses, pointing out to the maintenance of tubulin in the polymerized state as the appropriate condition for aggregation. Cytochalasin B, an actin-like filament disrupter, diminished the aggregating responses to the hormone, with no change in the slope of the regression curve, indicating that these elements take part in the process and that cytosolic calcium rise, sol/gel transformations and endoplasmic reticulum motility may well play an important role in granule migration. It is suggested that microtubules are steadily polymerized as a requirement for pigment aggregation and that process is biphasic, the initial phase being dependent on the microtubule integrity.
Tuma
M C
MC
Department of Physiology, NAPIG, USP, Brazil.
Josefsson
L
L
Castrucci
A M
AM
D000818:Animals; D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology; D002856:Chromatophores / Q000187:drug effects* / Q000378:metabolism; D003078:Colchicine / Q000494:pharmacology; D003571:Cytochalasin B / Q000494:pharmacology; D003599:Cytoskeleton / Q000187:drug effects / Q000502:physiology*; D004121:Dimethyl Sulfoxide; D004305:Dose-Response Relationship, Drug; D006074:Gout Suppressants / Q000494:pharmacology; D007447:Invertebrate Hormones / Q000494:pharmacology*; D008162:Lumicolchicines / Q000494:pharmacology; D017239:Paclitaxel / Q000494:pharmacology; D033541:Palaemonidae / Q000166:cytology; D010860:Pigments, Biological / Q000378:metabolism; D012044:Regression Analysis; D013696:Temperature; D014747:Vinblastine / Q000494:pharmacology
D000972:Antineoplastic Agents, Phytogenic; D006074:Gout Suppressants; D007447:Invertebrate Hormones; D008162:Lumicolchicines; D010860:Pigments, Biological; D003571:Cytochalasin B; C042109:lumicolchicine; D014747:Vinblastine; D017239:Paclitaxel; D003078:Colchicine; D004121:Dimethyl Sulfoxide