1. Department of Biology, New York University, 100 Washington Square East, New York, New York 10003, USA
2. Institute of Human Genetics, University of Utah, Salt Lake City, Utah 84112, USA
3. These authors contributed equally to this work.

Correspondence to: Christine Rushlow¹ Correspondence and requests for materials should be addressed to C.R. (Email: chris.rushlow@nyu.edu).

Abstract

In all animals, the initial events of embryogenesis are controlled by maternal gene products that are deposited into the developing oocyte. At some point after fertilization, control of embryogenesis is transferred to the zygotic genome in a process called the maternal-to-zygotic transition. During this time, many maternal RNAs are degraded and transcription of zygotic RNAs ensues¹. There is a long-standing question as to which factors regulate these events. The recent findings that microRNAs^{2, 3} and Smaug⁴ mediate maternal transcript degradation have shed new light on this aspect of the problem. However, the transcription factor(s) that activate the zygotic genome remain elusive. The discovery that many of the early transcribed genes in Drosophila share a cis-regulatory heptamer motif, CAGGTAG and related sequences^{5, 6}, collectively referred to as TAGteam sites⁵ raised the possibility that a dedicated transcription factor could interact with these sites to activate transcription. Here we report that the zinc-finger protein Zelda (Zld; Zinc-finger early Drosophila activator) binds specifically to these sites and is capable of activating transcription in transient transfection assays. Mutant embryos lacking zld are defective in cellular blastoderm formation, and fail to activate many genes essential for cellularization, sex determination and pattern formation. Global expression profiling confirmed that Zld has an important role in the activation of the early zygotic genome and suggests that Zld may also regulate maternal RNA degradation during the maternal-to-zygotic transition.

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