High impact information on slpr

• From these analyses we confirm that failure of dorsal closure is the null phenotype in slpr germline clones [1].
• In addition, there is a functional maternal contribution, which can suffice for embryogenesis in the zygotic null mutant, but rarely suffices for pupal metamorphosis, revealing later functions for slpr as the maternal contribution is depleted [1].
• To further define the specific functions of SLPR, we analyzed the phenotypic consequences of slpr loss and gain of function throughout development, using a semiviable maternal-effect allele and wild-type or dominant-negative transgenes [1].
• Drosophila mixed lineage kinase/slipper, a missing biochemical link in Drosophila JNK signaling [2].
• Further, dMLK directly phosphorylates Hep, dMKK4 and also their mammalian counterparts, MKK7 and SEK1, in an in vitro kinase assay [2].

Anatomical context of slpr

• In situ hybridization and reverse transcriptase polymerase chain reaction (RT-PCR) analysis revealed that dMLK is expressed in early embryonic stages, adult brain and thorax [2].

Associations of slpr with chemical compounds

• The protein structure analysis of dMLK/slipper revealed, in addition to the conserved domains, a stretch of glutamine in the amino terminus and an asparagine-threonine stretch at the carboxy-terminus [2].

References