Photoreceptor nuclei in the Drosophila eye undergo developmentally regulated migrations. Nuclear migration is known to require the perinuclear protein Klarsicht, but the function of Klarsicht has been obscure. Here, we show that Klarsicht is required for connecting the microtubule organizing center (MTOC) to the nucleus. In addition, in a genetic screen for klarsicht-interacting genes, we identified Lam Dm(0), which encodes nuclear lamin. We find that, like Klarsicht, lamin is required for photoreceptor nuclear migration and for nuclear attachment to the MTOC. Moreover, perinuclear localization of Klarsicht requires lamin. We propose that nuclear migration requires linkage of the MTOC to the nucleus through an interaction between microtubules, Klarsicht, and lamin. The Klarsicht/lamin interaction provides a framework for understanding the mechanistic basis of human laminopathies.
Drosophila klarsicht null mutants were viable and fertile, demonstrating that klarsicht is essential only for specific motor protein functions. Perinuclear localization of Klarsicht protein indicates that Klarsicht has a direct mechanical role in nuclear migration. Taken together with the finding that the minus ends of the microtubules are associated with the photoreceptor nuclei, the observation that Klarsicht is largely perinuclear supports the idea that Klarsicht associates with dynein, consistent with a model in which Klarsicht assists dynein in 'reeling in' the nucleus.
While a number of transcription factors that are likely to play a role in cardiac differentiation have recently been described, the signals that lead to the expression of these factors remains poorly understood. Here we report that exposure of Xenopus embryos to continuous low levels of all-trans retinoic acid (RA), starting at the time of neural fold closure, blocks expression of myocardial differentiation markers. The development of the remainder of the embryo is relatively normal, suggesting that retinoic acid can act rather specifically on myocardial precursors. Indeed, the pattern of endocardial gene expression appears to remain unaffected by RA treatment. Although RA blocks myocardial gene expression, a superficially normal heart tube forms. The heart tube, however, fails to loop during subsequent development and never forms beating tissue. The effect of RA treatment on expression of myocardial genes is developmental stage dependent, since no influence is observed after myocardial differentiation has commenced. These data indicate that a vital component of the myocardial determination pathway is sensitive to retinoid signaling. ᭧ 1997 Academic Press 1 To whom correspondence and reprint requests should be addressed. ers and a larger heart results. It seems likely that the ele-205
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