Reversible suppression of protein synthesis in concert with polysome disaggregation during anoxia exposure in Littorina littorea.
Many marine invertebrates can live without oxygen for long periods of time, a capacity that is facilitated by the ability to suppress metabolic rate in anoxia to a value that is typically less than 10% of the normal aerobic rate. The present study demonstrates that a reduction in the rate of protein synthesis is one factor in the overall anoxia-induced metabolic suppression in the marine snail, Littorina littorea. The rate of [3H]leucine incorporation into newly translated protein in hepatopancreas isolated from 48 h anoxic snails was determined to be 49% relative to normoxic controls. However, protein concentration in hepatopancreas did not change during anoxia, suggesting a coordinated suppression of net protein turnover. Analysis of hepatopancreas samples from snails exposed to 24-72 h anoxia showed a gradual disaggregation of polysomes into monosomes. A re-aggregation of monosomes into polysomes was observed after 3 h of aerobic recovery. Analysis of fractions from the ribosome profile using radiolabeled probe to detect alpha-tubulin transcripts confirmed a general decrease in protein translation during anoxia exposure (transcript association with polysomes decreased) with a reversal during aerobic recovery. Western blotting of hepatopancreas samples from normoxic, 24 h anoxic, and 1 h aerobic recovered snails demonstrated that eIF-2alpha is substantially phosphorylated during anoxia exposure and dephosphorylated during normoxia and aerobic recovery, suggesting a decrease in translation initiation during anoxia exposure. These results suggest that metabolic suppression during anoxia exposure in L. littorea involves a decrease in protein translation.
Larade
Kevin
K
Department of Biology and Institute of Biochemistry, Carleton University, Ottawa, Ontario, Canada.
Storey
Kenneth B
KB
D000818:Animals; D015153:Blotting, Western; D015180:Electrophoresis, Gel, Two-Dimensional; D015852:Eukaryotic Initiation Factor-2 / Q000032:analysis; D000860:Hypoxia / Q000378:metabolism*; D008974:Mollusca / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism*; D010100:Oxygen / Q000494:pharmacology; D011132:Polyribosomes / Q000187:drug effects / Q000378:metabolism*; D014176:Protein Biosynthesis / Q000187:drug effects; D011506:Proteins / Q000032:analysis; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013997:Time Factors; D014404:Tubulin / Q000096:biosynthesis / Q000235:genetics
D015852:Eukaryotic Initiation Factor-2; D011506:Proteins; D012333:RNA, Messenger; D014404:Tubulin; D010100:Oxygen