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Nucleic Acids Research, 1993, Vol. 21, No. 18 4372-4377
© 1993

MOLECULAR BIOLOGY

The tyrosine phosphatase cdec25 selectively inhibitis transcription of the Xenopus oocyte-type tRNAtyrC gene

Wanda F. Reynolds*

La Jolla Cancer Research Foundation 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA

*To whom correspondence should be addressed

Received March 19, 1993. Revised July 6, 1993. Accepted July 6, 1993.

The Xenopus tyrosine tRNAtyrC (TyrC) genes are developmentally regulated. These multicopy genes are expressed In early oocytes and Inactivated as oocytes reach maturity (1). As shown here, this developmental regulation can be reproduced In vitro In extracts of early and late stage oocytes: the TyrC gene Is transcribed in early oocyte extracts but Is virtually Inactive in mature oocyte extracts. The inability to transcribe the TyrC gene Is not due to the lack of functional pol III transcrlptlonal components, since the somatic-type, TyrD gene Is fully active In mature oocyte extracts. Instead, the loss of TyrC transcription appears to be due to a change In the template specificity of transcription factor TF1IIC: addition of TFIIIC from immature extracts restores TyrC transcription In mature extracts. In mixtures of immature and mature extracts, the transcrlptlonal activity of the TyrC gene Is reduced. The presence of sodium vanadate, an inhibitor of tyrosine phosphatases, increases the level of TyrC transcription In the extract mixtures. Also, cdc25 phosphatase treatment of immature extracts causes a decrease In TyrC transcription which is reversed by addition of exogenous TFIIIC. These findings Indicate that changes in phosphorylatlon state alters the template specificity of TFIIIC leading to the selective inactivation of oocyte type TyrC genes.


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