Reference Report

Reference
Citation	Sawamoto, K., Winge, P., Koyama, S., Hirota, Y., Yamada, C., Miyao, S., Yoshikawa, S., Jin, M.H., Kikuchi, A., Okano, H. (1999). The Drosophila Ral GTPase regulates developmental cell shape changes through the Jun NH(2)-terminal kinase pathway. J. Cell Biol. 146(2): 361--372. (Export to RIS)
FlyBase ID	FBrf0110725
Publication Type	Research paper
PubMed ID	10427090
PubMed Abstract	The Ral GTPase is activated by RalGDS, which is one of the effector proteins for Ras. Previous studies have suggested that Ral might function to regulate the cytoskeleton; however, its in vivo function is unknown. We have identified a Drosophila homologue of Ral that is widely expressed during embryogenesis and imaginal disc development. Two mutant Drosophila Ral (DRal) proteins, DRal(G20V) and DRal(S25N), were generated and analyzed for nucleotide binding and GTPase activity. The biochemical analyses demonstrated that DRal(G20V) and DRal(S25N) act as constitutively active and dominant negative mutants, respectively. Overexpression of the wild-type DRal did not cause any visible phenotype, whereas DRal(G20V) and DRal(S25N) mutants caused defects in the development of various tissues including the cuticular surface, which is covered by parallel arrays of polarized structures such as hairs and sensory bristles. The dominant negative DRal protein caused defects in the development of hairs and bristles. These phenotypes were genetically suppressed by loss of function mutations of hemipterous and basket, encoding Drosophila Jun NH(2)-terminal kinase kinase (JNKK) and Jun NH(2)-terminal kinase (JNK), respectively. Expression of the constitutively active DRal protein caused defects in the process of dorsal closure during embryogenesis and inhibited the phosphorylation of JNK in cultured S2 cells. These results indicate that DRal regulates developmental cell shape changes through the JNK pathway.
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Language of Publication	English
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Publication Type	Journal
Abbreviation	J. Cell Biol.
Title	Journal of Cell Biology
Publication Year	1966-
ISBN/ISSN	0021-9525
Data from Reference
Aberrations (2)
	Df(3L)Ar14-8 Df(3L)pbl-X1
Alleles (31)
	bsk¹ bsk² bsk^flp147E Cdc42¹ Dsor1^Gp158 Dsor1^Su1 hep¹ hep^r75 mbt^P1 mbt^P2 phl¹ Rala^{G20V.Scer\UAS} Rala^{S25N.Scer\UAS} Rala^Scer\UAS.cSa Ras85D^e2F Rho1^Df236 Rho1^Df903 Rho1^k07903 rl⁹ rl^Su23 Scer\GAL4^69B Scer\GAL4^Act5C.PHb Scer\GAL4^Act5C.PI Scer\GAL4^arm.PS Scer\GAL4^da.G32 Scer\GAL4^GMR.PF Scer\GAL4^LE Scer\GAL4^pnr-MD237 Scer\GAL4^sca-537.4 Scer\GAL4^unspecified w^+mC
Constructs (7)
	P{Act5C-GAL4} P{GAL4-arm.S} P{GAL4-da.G32} P{GAL4-ninaE.GMR} P{UAS-Rala.G20V} P{UAS-Rala.S25N} P{UAS-Rala.S}
Genes (15)
	bsk Cdc42 Dsor1 futsch hep mbt phl Rac1 Rac2 Rala Ras85D Rho1 rl Scer\GAL4 w
Insertions (4)
	P{GAL4}LE P{GawB}69B P{GawB}pnr^MD237 P{GawB}sca^537.4