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Redox signaling in the growth and development of colonial hydroids

Neil W. Blackstone

Department of Biological Sciences, Northern Illinois University, DeKalb, IL 60115, USA

View larger version (20K): [in a new window]   Fig. 1. Schemata of the mitochondrial electron transport chain, showing complexes I-V, coenzyme Q and cytochrome c. Small arrows trace the flow of electrons from NADH and FADH2 to oxygen. Large arrows show the extrusion of protons (H+) by complexes I, III and IV and the return of protons to the matrix via complex V, triggering the assembly of ATP (dashed arrow). Red stars indicate the two major sites of reactive oxygen formation. Uncouplers of oxidative phosphorylation allow electrons to return to the matrix without passing through complex V (after Blackstone and Kirkwood, 2003).

View larger version (91K): [in a new window]   Fig. 6. Images of an approximately 50 µmx150 µm region at the base of two living polyps [treatments: (A) antimycin, (B) rotenone]. Each image shows emission at fluorescein wavelengths after treatment with 2',7'-dichlorofluorescin diacetate (H2DCFDA). The principal signal is from clusters of mitochondria surrounding muscle fibers in epitheliomuscular cells (approximately 3-4 µm in diameter). After background correction, there is a slight difference in the luminance (given in greyscale) of these objects in these two images; A=1485, B=1345 (grayscale from 0 to 4095; compare with Fig. 7).

View larger version (13K): [in a new window]   Fig. 2. Rate of decline in oxygen concentration for P. carnea colonies before (squares) and after (circles) treatment with (A) 1 µmol l-1 CCCP, (B) 1 µmol l-1 antimycin A1 and (C) 10 µmol l-1 rotenone. For five colonies of each treatment, inset plots show the mean ± S.E.M. of the before/after difference in the rate of decline in oxygen concentration, where this decline is measured by the least-squared slope of oxygen concentration versus time. This difference in rate was significantly negative for (A), i.e. the oxygen uptake increased after treatment, and significantly positive for (B) and (C), i.e. the oxygen uptake decreased after treatment.

View larger version (15K): [in a new window]   Fig. 3. Bivariate scatterplots of the amount of stolon development (inversely correlated to empty area/total surface area) and the amount of polyp development (polyp area/total surface area) for genetically identical P. carnea colonies at the initiation of medusa production. Squares, treated with 1 µmol l-1 antimycin; circles, treated with 1 µmol l-1 m-chlorophenylhydrazone (CCCP); triangles, treated with 0.08% dimethyl sulfoxide; diamonds, treated with 10 µmol l-1 rotenone.

View larger version (169K): [in a new window]   Fig. 4. Images of genetically identical colonies of P. carnea growing on 15 mm diameter glass cover slips at the initiation of medusa production. Treatments are as in Fig. 3: (A) antimycin, (B) DMSO control, (C) CCCP and (D) rotenone.

View larger version (16K): [in a new window]   Fig. 5. Mean ± S.E.M. of the average size of the areas of empty cover slip within the colonies (`inner area') for the colonies treated as in Fig. 3.

View larger version (17K): [in a new window]   Fig. 7. Mean ± S.E.M. luminance (grayscale from 0 to 4095) for three polyps per replicate colony. Colonies were treated with either antimycin (open bars) or rotenone (filled bars).