Androgen Receptor Antagonists we tested whether k RasV12 DHR4
Nnte The nucleus, we tested whether k RasV12 DHR4 Nnte nuclear localization sequence in cells of larval fatty substances Body where DHR4 was shown limited to the kernel as soon as the translation took place, at least in L2 and L3 larvae are abolished. If we targeted the expression of fatty substances in the UAS RasV12 Body with Cg Gal4, we found to be virtually non-existent DHR4 cores and strong in the cytoplasm can be enriched, indicating that Ras is constitutively active sufficient to retention of the cytoplasmic DHR4 auszul sen. These best results Term our results from the PG, which convincingly demonstrate that the nucleocytoplasmic distribution DHR4 controlled Controlled by PTTH signaling.
DHR4 overexpression in PG rescues RasV12 Dependence Ph Phenotypes of Ras DHR4 is fascinating because RasV12 is best of our knowledge, the only other known genetic Ver Change au Outside the DHR41 mutation that results in the development of the larvae and pupae slightly faster . There is also the presence of larvae in RasV12 dwarf animals. These results are consistent with our observation that RasV12 DHR4 prevents accumulate in the nucleus, thereby disrupting its nuclear capabilities Similar DHR41 mutants or RNAi animals DHR4. Based on this observation, k Can we predict some of the effects of RasV12 blocked k Nnte when the H He DHR4 of proteins Erh Ht be in the same fabric. We asked if was DHR4 epistatic Ras, or more precisely, if we RasV12 Ph Phenotypes by overexpression DHR4 k specifically save the PG-induced Nnte.
First, we determined the average L Length of the formation, if puparium RasV12 or DHR4, or both, are expressed in the ring groove with P0206 Gal4 driver. As mentioned Hnt, 5% to 10% P0206.DHR4 / 2 larvae reach prepupal stage that allows us to determine its synchronization profile. As previously reported by others, P0206.RasV12 animals develop much faster than in the controls before the start of embroidered by the prepupae, 20 h, however P0206.DHR4 / 2 with a form prepupae, 20 hour delay Delay compared with controls. However, when RasV12 and DHR4 expressed together in the left, we see rescue the normal schedule of pupation and the mortality t DHR4 partial mediation. Since RasV12 overexpression in Ph Hyperproliferative phenotype, we wondered whether this aspect of the Ras activity T could be rescued by overexpression DHR4.
For this purpose we have investigated the morphology of the gland ring isolated from L3 larvae RasV12 expression and / or staged DHR4. P0206.RasV12 larval ring glands very large, w During DHR4 expression using the same driver results in slightly smaller ring glands compared to the control group. It is important when co DHR4 is expressed seems to RasV12, hyperproliferation of the gland ring to be repressed, which strongly suggests that the increased FITTINGS mirror DHR4 tissue blocks the activity t of Ras. Nucleon Re localization of ERK / MAPK and DHR4 inverse PTTH acts on PG ultimately the activation of ERK, a MAP kinase correlated with phosphorylation. After the activation of ERK to the nucleus and can phosphorylate nuclear target proteins Such as transcription factors and other kinases. Since r PTTH is the key for the induction of biosynthesis of ecdysone and seems DHR4 the inverse function, we predict that the Nukleaseaktivit t PTTH remove .