Reversible re‐fusion of frog blastomeres and additional cleavage effects of chloramphenicol and other respiratory inhibitors

Abstract

AbstractChloramphenicol (CAP) produced an unusual cleavage anomaly in Rana pipiens embryos involving re‐fusion of normal looking 6 to 12 hour blastomeres into irregularly shaped syncytial mounds. This occurred whether the CAP was added then or earlier. The condition was usually terminal, but often at lower doses or following CAP removal the mounts re‐cleaved and the embryos resumed development. Preliminary histological verification of blastomere fusion has been obtained.The same anomaly was produced by two other inhibitors, rotenone and the L‐isomer of CAP. These are without effect on mitochondrial protein synthesis in other systems but do share with high doses of D‐CAP a direct inhibition of respiration at the NADH oxidase level. Another such inhibitor, amytal, failed to affect cleavage, presumably because of poor penetration. Instead, amytal produced uniform developmental arrest at later stages characteristic for each dose. Similar but less uniform results were obtained with lower doses of D‐ and L‐CAP, rotenone, cyanide, and dinitrophenol. All of these, however, also produced cleavage arrest at higher doses, including prevention of first cleavage altogether at high enough concentrations of each.This disagrees with the older literature in the case of cyanide, to which early cleavage is purported to be insensitive and the onset of gastrulation unusually sensitive. There is also an apparent conflict between our cyanide‐rotenonechloramphenicol results, suggesting that cleavage is dependent on respiration, and the work of others on cleavage under anaerobiosis, suggesting not. Several hypotheses which would resolve this conflict, including that of an oxidative reserve in the eggs, are presented and discussed.