RNA:RNA interaction can enhance RNA localization in Drosophila oocytes.

RNA localization is a key mechanism for targeting proteins to particular subcellular domains. Sequences necessary and sufficient for localization have been identified, but little is known about factors that affect its kinetics. Transcripts of gurken and the I factor, a non-LTR retrotransposon, colocalize at the nucleus in the dorso-antero corner of the Drosophila oocyte directed by localization signals, the GLS and ILS. I factor RNA localizes faster than gurken after injection into oocytes, due to a difference in the intrinsic localization ability of the GLS and ILS. The kinetics of localization of RNA containing the ILS are enhanced by the presence of a stem-loop, the A loop. This acts as an RNA:RNA interaction element in vivo and in vitro, and stimulates localization of RNA containing other localization signals. RNA:RNA interaction may be a general mechanism for modulating RNA localization and could allow an mRNA that lacks a localization signal to hitchhike on another RNA that has one.

Requirement for downregulation of kreisler during late patterning of the hindbrain.

Pattern formation in the hindbrain is governed by a segmentation process that provides the basis for the organisation of cranial motor nerves. A cascade of transcriptional activators, including the bZIP transcription factor encoded by the kreisler gene controls this segmentation process. In kreisler mutants, r5 fails to form and this correlates with abnormalities in the neuroanatomical organisation of the hindbrain. Studies of Hox gene regulation suggest that kreisler may regulate the identity as well as the formation of r5, but such a role cannot be detected in kreisler mutants since r5 is absent. To gain further insights into the function of kreisler we have generated transgenic mice in which kreisler is ectopically expressed in r3 and for an extended period in r5. In these transgenic mice, the Fgf3, Krox20, Hoxa3 and Hoxb3 genes have ectopic or prolonged expression domains in r3, indicating that it acquires molecular characteristics of r5. Prolonged kreisler expression subsequently causes morphological alterations of r3/r5 that are due to an inhibition of neuronal differentiation and migration from the ventricular zone to form the mantle layer. We find that these alterations in r5 correlate with an arrest of facial branchiomotor neurone migration from r4 into the caudal hindbrain, which is possibly due to the deficiency in the mantle layer through which they normally migrate. We propose that the requirement for the downregulation of segmental kreisler expression prior to neuronal differentiation reflects the stage-specific roles of this gene and its targets.