Publication Date:
2016-08-23
Description:
The excretion of nitrogenous waste products in the form of ammonia
(NH3) and ammonium (NH4
+) is a fundamental process in aquatic
organisms. For mytilid bivalves, little is known about the mechanisms
and sites of excretion. This study investigated the localization and the
mechanisms of ammonia excretion in mytilid mussels. An Rh protein
was found to be abundantly expressed in the apical cell membrane of
the plicate organ, which was previously described as a solely
respiratory organ. The Rh protein was also expressed in the gill,
although at significantly lower concentrations, but was not detectable
in mussel kidney. Furthermore, NH3/NH4
+ was not enriched in the
urine, suggesting that kidneys are not involved in active NH3/NH4
+
excretion. Exposure to elevated seawater pH of 8.5 transiently
reduced NH3/NH4
+ excretion rates, but they returned to control values
following 24 h acclimation. These mussels had increased abundance
of V-type H+-ATPase in the apical membranes of plicate organ cells;
however, NH3/NH4
+ excretion rates were not affected by the V-type
H+-ATPase specific inhibitor concanamycin A (100 nmol l−1). In
contrast, inhibition of ciliary beating with dopamine and increased
seawater viscosity significantly reduced NH3 excretion rates under
control pH (8.0). These results suggest that NH3/NH4+ excretion in
mytilid mussels takes place by passive NH3 diffusion across
respiratory epithelia via the Rh protein, facilitated by the water
current produced for filter feeding, which prevents accumulation of
NH3 in the boundary layer. This mechanism would be energy efficient
for sessile organisms, as they already generate water currents for
filter feeding.
Repository Name:
EPIC Alfred Wegener Institut
Type:
Article
,
peerRev
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