Regulatory factor for the transcription of the ribosomal genes in amphibian oocytes.

Abstract

AMPHIBIAN oocytes provide very convenient material for the study of the mechanisms that control ribosomal RNA synthesis because their pattern of ribosomal RNA synthesis does not change greatly during oogenesis. During the lampbrush stage of oogenesis (stage 4) more than 97 per cent of the RNA synthesized per unit time in the oocytes is ribosomal. This happens because the genes for ribosomal RNA are specifically amplified3–5 to such an extent that the oocyte nucleus (germinal vesicle) has an rDNA content approximately 1,500 times more than the haploid amount4. On the other hand, in mature oocytes (stage 6) no ribosomal RNA is synthesized1,2, although the extra copies of the ribosomal cistrons are still present. There must therefore be a mechanism in these cells which turns off ribosomal RNA synthesis. It should also be remembered that ribosomal RNA synthesis resumes only after the embryo has reached gastrulation6,7. Furthermore, the cytoplasmic environment in the egg and in the pre-gastrula embryo is such that when nuclei from neurula endoderm cells, active in ribosomal RNA synthesis, are transplanted into enucleated eggs, they stop ribosomal RNA synthesis, although they synthesize DNA-like and soluble RNAs and are able to sustain normal development of the embryo. Ribosomal RNA synthesis in the nuclear transplanted embryos resumes only at gastrulation8. It has been suggested9,10 that this cytoplasmic control of the pattern of nuclear transcription could be mediated through a factor which specifically inhibits ribosomal RNA synthesis.