A pair of pyrene- and anthracene-based turn-on fluorescent probes (1 and 2, respectively) reported here can be easily synthesized in a single-step process and also exhibit outstanding sensing behavior toward hydrazine over various competing nucleophilic species and environmentally relevant ions. The probes display dramatic enhancements in the emission intensity with as high as 83- and 173-fold increases in the presence of hydrazine. Nitrogenous bases, thiols, and lanthanides do not interfere in the fluorometric detection. These probes enable the detection of hydrazine with the naked eye well below sub-ppm concentrations (ca. 30 ppb) with analytical detection limits of 5.4 ppb for 1 and 7.7 ppb for 2, which are far exceeded by the accepted lower limit for hydrazine (10 ppb) set by the US EPA. Simple paper strips based on these probes could be used for the detection of hydrazine even in the gas phase. Both of the probes could selectively detect hydrazine even in pond water samples efficiently. The probes were successfully applied to visualize, for the first time, accumulation of hydrazine in live fruit-fly larvae using epifluorescence microscopy. The novel and interesting detection mechanism, proposed on the basis of spectroscopic evidence and single crystal XRD results, indicates that the detection pathway proceeds via the initial step of a five-membered ring formation upon attack of the hydrazine, followed by a dehydration step for gaining aromaticity.
Gap junction (GJ) proteins, the primary constituents of GJ channels, are conserved determinants of patterning. Canonically, a GJ channel, made up of two hemi-channels contributed by the neighboring cells, facilitates transport of metabolites/ions. Here we demonstrate the involvement of GJ proteins during cuboidal to squamous epithelial transition displayed by the anterior follicle cells (AFCs) from Drosophila ovaries. Somatically derived AFCs stretch and flatten when the adjacent germline cells start increasing in size. GJ proteins, Innexin2 (Inx2) and Innexin4 (Inx4), functioning in the AFCs and germline respectively, promote the shape transformation by modulating calcium levels in the AFCs. Our observations suggest that alterations in calcium flux potentiate STAT activity to influence actomyosin-based cytoskeleton, possibly resulting in disassembly of adherens junctions. Our data have uncovered sequential molecular events underlying the cuboidal to squamous shape transition and offer unique insight into how GJ proteins expressed in the neighboring cells contribute to morphogenetic processes.
As collective cell migration is intimately involved in different aspects of metazoan development, molecular mechanisms underlying this process are being explored in a variety of developmental contexts. Border cell (BC) migration during oogenesis has emerged as an excellent genetic model for studying collective cell migration. BCs are of epithelial origin but acquire partial mesenchymal characteristics before migrating as a group towards the oocyte. Here, we report that insulin signaling modulates collective BC movement during oogenesis. Supporting the involvement of Insulin pathway, we demonstrate that compromising Insulin-like Receptor (InR) levels in BCs, inhibits their migration. Furthermore, we show that canonical Insulin signaling pathway components participate in this process. Interestingly, visualization of -depleted BC clusters, using time-lapse imaging, revealed a delay in detachment of BC clusters from the surrounding anterior follicle cells and altered protrusion dynamics. Lastly, based on genetic interactions between, the polarity determinant, and a regulatory subunit of Myosin (), we propose that Insulin signaling likely influences activity to engineer border cell detachment and subsequent movement via Myosin.
Epithelial morphogenesis plays an important role in form generation, organ development, and maintenance of adult tissues in the metazoans. Given its wide implication, aberrant morphogenesis is linked to severe developmental defects and in a few instances also associated with tumorigenesis. Employing the model of Drosophila oogenesis, we have examined the role of the evolutionary conserved Target of Rapamycin (TOR) kinase pathway, a known regulator of cell growth and size in mediating shape transition of cuboidal cells to squamous epithelial fate. Utilizing genetic tools, immunohistochemistry, and live cell imaging, we demonstrate that TOR signaling is active and required for epithelial morphogenesis during Drosophila oogenesis. Further, loss of function analyses indicates that non-canonical TOR signaling functions through PAR-1 to mediate the removal of lateral cell adhesion molecule, Fasciclin 2, to allow proper squamous cell morphogenesis. In addition, we demonstrate the effect of TOR through PAR-1 on cell shape transition is mediated via the modulation of endocytosis. Overall, our data give novel insight into how TOR signaling mediates cell shape transition during epithelial morphogenesis in the metazoans.
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