Slam protein dictates subcellular localization and translation of its own mRNA.

Many mRNAs specifically localize within the cytoplasm and are present in RNA-protein complexes. It is generally assumed that localization and complex formation of these RNAs are controlled by trans-acting proteins encoded by genes different than the RNAs themselves. Here, we analyze slow as molasses (slam) mRNA that prominently colocalizes with its encoded protein at the basal cortical compartment during cellularization. The functional implications of this striking colocalization have been unknown. Here, we show that slam mRNA translation is spatiotemporally controlled. We found that translation was largely restricted to the onset of cellularization when Slam protein levels at the basal domain sharply increase. slam mRNA was translated locally, at least partially, as not yet translated mRNA transiently accumulated at the basal region. Slam RNA accumulated at the basal domain only if Slam protein was present. Furthermore, a slam RNA with impaired localization but full coding capacity was only weakly translated. We detected a biochemical interaction of slam mRNA and protein as demonstrated by specific co-immunoprecipitation from embryonic lysate. The intimate relationship of slam mRNA and protein may constitute a positive feedback loop that facilitates and controls timely and rapid accumulation of Slam protein at the prospective basal region.

Chromatin-associated noncoding RNAs in development and inheritance.

Noncoding RNAs (ncRNAs) have emerged as crucial players in chromatin regulation. Their diversity allows them to partake in the regulation of numerous cellular processes across species. During development, long and short ncRNAs act in conjunction with each other where long ncRNAs (lncRNAs) are best understood in establishing appropriate gene expression patterns, while short ncRNAs (sRNAs) are known to establish constitutive heterochromatin and suppress mobile elements. Additionally, increasing evidence demonstrates roles of sRNAs in several typically lncRNA-mediated processes such as dosage compensation, indicating a complex regulatory network of noncoding RNAs. Together, various ncRNAs establish many mitotically heritable epigenetic marks during development. Additionally, they participate in mechanisms that regulate maintenance of these epigenetic marks during the lifespan of the organism. Interestingly, some epigenetic traits are transmitted to the next generation(s) via paramutations or transgenerational inheritance mediated by sRNAs. In this review, we give an overview of the various functions and regulations of ncRNAs and the mechanisms they employ in the establishment and maintenance of epigenetic marks and multi-generational transmission of epigenetic traits. WIREs RNA 2017, 8:e1435. doi: 10.1002/wrna.1435 For further resources related to this article, please visit the WIREs website.

Function and dynamics of slam in furrow formation in early Drosophila embryo.

The Drosophila embryo undergoes a developmental transition in the blastoderm stage switching from syncytial to cellular development. The cleavage furrow, which encloses nuclei into cells, is a prominent morphological feature of this transition. It is not clear how the pattern of the furrow array is defined and how zygotic genes trigger the formation and invagination of interphase furrows. A key to these questions is provided by the gene slam, which has been previously implicated in controlling furrow invagination. Here we investigate the null phenotype of slam, the dynamics of Slam protein, and its control by the recycling endosome. We find that slam is essential for furrow invagination during cellularisation and together with nullo, for specification of the furrow. During cellularisation, Slam marks first the furrow, which is derived from the metaphase furrow of the previous mitosis. Slightly later, Slam accumulates at new furrows between daughter cells early in interphase. Slam is stably associated with the furrow canal except for the onset of cellularisation as revealed by FRAP experiments. Restriction of Slam to the furrow canal and Slam mobility during cellularisation is controlled by the recycling endosome and centrosomes. We propose a three step model. The retracting metaphase furrow leaves an initial mark. This mark and the border between corresponding daughter nuclei are refined by vesicular transport away from pericentrosomal recycling endosome towards the margins of the somatic buds. Following the onset of zygotic gene expression, Slam and Nullo together stabilise this mark and Slam triggers invagination of the cleavage furrow.