Перегляд вихідного коду сторінки Anti-Wg staining in wing imaginal discs of control (A) or en-Gal4, UASwg-RNAi 3rd instar larvae (B). No staining is observed in the posterior compartment of discs that convey wg-RNAi

The JNK pathway is involved in both RBF- and RBFD253Ainduced apoptosis, as a result we can't exclude that the inhibition of RBFD253A-induced overgrowth phenotype is a consequence of the decrease of apoptosis in bsk-RNAi expressing and hepr75 contexts. In fact, RBFD253A-induced overgrowth phenotype could result from a misregulation of an apoptosis-induced proliferation procedure. But this cellular process, by which apoptotic cells encourage proliferation of encompassing living cells, also is dependent on the JNK pathway. In the same way in the literature, ``undead cells'', which are kept alive by the caspase inhibitor p35 right after induction of apoptosis by a pro-apoptotic gene, induce non-mobile autonomous proliferation by a persistent [http://eaamongolia.org/vanilla/discussion/156817/all-morphological-scientific-studies-were-performed-by-essential-imaging-utilizing-planapochromat-63 All morphological scientific studies have been performed by important imaging employing PlanApochromat 63x] activation of the JNK pathway [forty three,47,49,50,fifty one]. Because the JNK pathway is important for RBFD253A-induced overgrowth, it is achievable that this cleavageresistant form of RBF possesses an improved capacity to activate the JNK in a way that could increase the JNK non-apoptotic capabilities. Further investigation will be required to make clear the repercussions of the JNK pathway activation by RBF and RBFD253A, and why this activation could lead to diverse phenotypes. 1 could also hypothesize that RBF and RBFD253A do not activate the JNK pathway by way of the same upstream parts, which could guide to diverse outcomes. We showed that contrarily to what is observed in the presence of undead cells, RBFD253A-induced overgrowth does not need Wg action. In undead cells, the JNK pathway activation has been shown to lead to ectopic wg expression that is responsible for the noticed overgrowth [forty three,forty seven,49,52]. Furthermore, the secretion of Wg is not limited to undead cells, but also takes place in ``genuine'' apoptotic cells [53]. We hypothesized that RBFD253A-induced overgrowth could consequence from a misregulation of apoptosis-induced mobile proliferation through Wg signaling. We rejected this speculation since the inhibition of wg expression with a wg-RNAi construct, that in our experiment entirely abrogates the detection of wg protein, did not lessen overgrowth. Furthermore, the wg expression pattern in en.RBFD253A wing discs was different sort the pattern noticed in en.RBF, p35 discs that contained undead cells and exhibited common ectopic patches of wg-expressing cells. In en.RBFD253A and ptc.RBFD253A wing discs, more cells seemed to express wg, leading to an enlargement or a deformation of the sample, but we did not observe ectopic patches of wg expression.