Regulation of a serine protease homolog by the JNK pathway during thoracic development ofDrosophila melanogaster

Abstract

HighlightsScarface is up-regulated in peripodial epithelium and peripodial stalk cells in wing disc.Overexpression of JNK pathway causes up-regulation of scarface.Down regulation of JNK pathway results in down regulation of scarface.Scarface knockdown in wing disc phenocopies JNK pathway defect.

Ligand-Bound GeneSwitch Causes Developmental Aberrations inDrosophilathat Are Alleviated by the Alternative Oxidase

“…Defects in JNK signaling also underlie wing defects and leg malformations ( Kirchner et al 2007 ), and have been implicated in midline closure defects in mammals ( Chi et al 2005 ; Zhu et al 2016 ). Cleft-thorax can result both from downregulation of effectors of JNK signaling, such as the serine protease scarface ( Srivastava and Dong 2015 ), or from mutations in receptor tyrosine kinase Pvr ( Garlena et al 2015 ), an upstream JNK pathway activator ( Ishimaru et al 2004 ; Igaki 2009 ). Thoracic closure also depends on downstream targets such as proteins implicated in cytokinesis and cell adhesion ( Sfregola 2014 ), as well as intracellular protein trafficking ( Thomas et al 2009 ).…”

Expression of the Alternative Oxidase Influences Jun N-Terminal Kinase Signaling and Cell Migration

“…Cleft thorax is produced by mutant alleles of the JNK kinase (JNKK) hemipterous ( hep ) ( 30 ) or of the AP-1 subunit kayak ( kay ; the Drosophila ortholog of mammalian c- Fos ) ( 31 ). The use of pnr -GAL4 or other drivers to bring about the local downregulation of JNK targets, such as scarface (serine protease) ( 32 ), or overexpression of the AP-1 target puckered ( puc ; a phosphatase regulator of JNK via a negative feedback loop) ( 33 ) or the tissue inhibitor of metalloproteases ( Timp ) ( 34 ) can also produce cleft thorax, while downregulation of puc can rescue cleft thorax caused by mutations of hep ( 30 ). One key target of JNK in dorsal closure ( 35 , 36 ) is the transforming growth factor β family member decapentaplegic (dpp).…”

A serine protease homologue Bombyx mori scarface induces a short and fat body shape in silkworm

“…The SPH serine proteases lack the catalytic triad at their active centres and are thought to have novel functions (Pils & Schultz, 2004). For example, a novel serine protease Protease serine56, a trypsin serine proteaselike protein (PRSS56) is responsible for nanophthalmos in humans (Orr et al, 2011), the masquerade (mas) mutation destroys the somatic muscle attachment in Drosophila embryos (Murugasu-Oei et al, 1995, 1996, Stubble affects the organization of microfilament bundles during bristle morphogenesis (Hammonds & Fristrom, 2006) and Dmscarface (scarface homologue in Drosophila) plays an important role in the development of thorax and participates in the dorsal closure of the Drosophila embryo (Rousset et al, 2010;Srivastava and Dong, 2015). These studies imply that the SPH genes are involved in external morphological characteristics of body shape.…”