Insect immune defense is mainly based on humoral factors like antimicrobial peptides (AMPs) that kill the pathogens directly [1] or on cellular processes involving phagocytosis and encapsulation by hemocytes [2]. In Drosophila, the Toll pathway (activated by fungi and gram-positive bacteria) and the lmd pathway (activated by gram-negative bacteria) lead to the synthesis of AMPs [3]. But AMP genes are also regulated without pathogenic challenge, e.g., by aging, circadian rhythms, and mating [4-8]. Here, we show that AMP genes are differentially expressed in mated females. Metchnikowin (Mtk) expression is strongly stimulated in the first 6 hr after mating. Sex-peptide (SP), a male seminal peptide transferred during copulation, is the major agent eliciting transcription of Mtk and of other AMP genes. Both pathways are needed for Mtk induction by SP. Furthermore, SP induces additional AMP genes via the Toll (Drosomycin) and the Imd (Diptericin) pathways. SP affects the Toll pathway at or upstream of the gene spatzle, the Imd pathway at or upstream of the gene imd. Mating may physically damage females and pathogens may be transferred [9]. Thus, endogenous stimulation of AMP transcription by SP at mating might be considered as a preventive step to encounter putative immunogenic attacks.

Centrosomes are major determinants of mitotic spindle structure, but the mechanisms regulating their behavior remain poorly understood. The spd-2 gene of C. elegans is required for centrosome assembly or “maturation.” Here we show that spd-2 encodes a coiled-coil protein that localizes within pericentriolar material (PCM) and in the immediate vicinity of centrioles. During maturation, SPD-2 gradually accumulates at the centrosome in a manner that is partially dependent on Aurora-A kinase and cytoplasmic dynein. Interestingly, SPD-2 interacts genetically with dynein heavy chain and SPD-5, another coiled-coil protein required for centrosome maturation. SPD-2 and SPD-5 are codependent for localization to the PCM, but SPD-2 localizes to centrioles independently of SPD-5. Surprisingly, we also find that SPD-2 is required for centrosome duplication and genetically interacts with ZYG-1, a kinase required for duplication. Thus, we have identified SPD-2 as a factor critical for the two basic functions of the centrosome—microtubule organization and duplication.

Early embryonic development involves complex events such as the regulation of cell division and the establishment of embryonic polarity. To identify genes involved in these events, we collected four‐dimensional time‐lapse video recordings of the first three cell divisions and analysed terminal phenotypes after RNA interference of 147 embryonic lethal genes previously identified in a systematic screen of Caenorhabditis elegans chromosome I. Over half gave defects in early processes such as meiosis, the assembly or position of the first mitotic spindle, cytokinesis, and proper nuclear positioning. For some phenotypic classes, the majority of genes are involved in a shared biochemical process. In addition, we identified loss‐of‐function phenotypes for genes of unknown function, but for which homologues exist in other organisms, shedding light on the function of these uncharacterized genes. When applied to the whole genome, this approach should identify the vast majority of genes required for early cell processes, paving the way for a greatly improved understanding of these processes and their regulation at the molecular level.