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First published online December 2, 2005
Journal of Experimental Biology 208, 4671-4678 (2005)
Published by The Company of Biologists 2005
doi: 10.1242/jeb.01934
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To DGC or not to DGC: oxygen guarding in the termite Zootermopsis nevadensis (Isoptera: Termopsidae)

John R. B. Lighton1,* and Elizabeth A. Ottesen2

1 Department of Biology, University of Nevada at Las Vegas, NV 89154-4004, USA
2 California Institute of Technology, Biology Division, Pasadena, CA 91125, USA



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Fig. 1. Conceptual diagram of the experimental setup. PE-temp, Peltier Effect temperature cabinet and controller; H, water reservoir (for air hydration); RC, respirometer chamber; GS1–GS4, gas changeover solenoids under computer control via ExpeData; MFC, mass flow control valve and electronics unit; S, scrubber. Large scrubber=Drierite/Ascarite/Drierite for removal of H2O and CO2 from normoxic air; small scrubber=Ascarite for removal of trace CO2 from the selected gas stream. NV, needle valve; CO2, CO2 analyzer; MFM, mass flow meter; X, closed (no gasflow). The light emitter and sensor used for detection of activity in the respirometry chamber are not shown. See text for details.

 


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Fig. 2. Typical recording, showing the response of a termite to hyperoxia (switch to 100% O2; see indicator on graph) with a subsequent return to normoxia (switch to 21% O2; see indicator on graph) at 15°C. The oxygen guarding response, resulting in a transient decline of CO2 emission rates, is clearly visible, as is a compensatory transient emission of CO2 after re-establishment of normoxia. The body mass of this termite was 0.0122 g. Baselines are shown at the start and end of the recording. See text for details.

 


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Fig. 3. Mass scaling of rate of CO2 emission (VCO2 in µl h–1) in Zootermopsis nevadensis prior to hyperoxia (open circles), shortly after exposure to hyperoxia (closed circles), ca. 30 min after exposure to hyperoxia (open squares), shortly after re-establishment of normoxia (closed squares) and ca. 30 min after re-establishment of normoxia (crosses); N=21, all at 15°C. By ANCOVA, all lines share a common slope or mass scaling exponent of 0.688(F[4,95]=0.59; P>0.3). The intercepts, however, differed significantly (F[4,99]=109.7, P<10–12). The mass scaling coefficients are, respectively, 89.7, 27.0, 69.8, 197.7, and 53.1 with VCO2. in units of µl h–1.

 


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Fig. 4. The relation between equilibrium, pre-treatment VCO2 (µl h–1) and the lowest 60 s of hyperoxic VCO2 in the dampwood termite Zootermopsis nevadensis; N=21, at 15°C. Pre-treatment VCO2 explains 75% of hyperoxic VCO2 variance; hyperoxic VCO2=0.46+0.258±0.034 (pre-treatment VCO2), F[1,19]=56.7, P<10–6.

 


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Fig. 5. The relation between equilibrium, pre-treatment VCO2 (µl h–1) and the equilibrium VCO2 during prolonged exposure to hyperoxia in the dampwood termite Zootermopsis nevadensis; N=21, at 15°C. Pre-treatment VCO2 explains 79% of equilibrium VCO2 variance during hyperoxia; equilibrium hyperoxic VCO2=0.33+0.802±0.094 (pre-treatment VCO2, F[1,19]=72.9, P<10–6. The slope is marginally significantly below 1.0 (P<0.05). See text for details.

 


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Fig. 6. The relation between equilibrium, pre-treatment VCO2 (µl h–1) and the equilibrium recovery VCO2 after returning to normoxia (following prolonged exposure to hyperoxia) in the dampwood termite Zootermopsis nevadensis; N=21, at 15°C. Pre-treatment VCO2 explains 87% of recovery VCO2 variance during hyperoxia; recovery VCO2=0.28+0.576±0.050 (pre-treatment VCO2), F[1,19]=133, P<10–6. See text for details.

 


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Fig. 7. The relation between the volume of CO2 withheld immediately following exposure to hyperoxia (CO2 deficit), and the volume (µl) of CO2 emitted immediately after restoration of normoxia (CO2 surplus), N=21, at 15°C. CO2 deficit explains 58% of CO2 surplus variance. CO2 surplus=0.81–1.353±0.264 CO2 deficit; F[1,19]=26.2, P<10–6. The slope of this relation does not differ significantly from 1.0 (P=0.1). See text for details.

 

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© The Company of Biologists Ltd 2005