Phantom / phm antibody

Principal name

Phantom / phm antibody

Alternative names for Phantom / phm antibody

Dmphm, Cyp306a1, CYPCCCVIA1, CG6578, Cytochrome P450 306a1

SwissProt ID

Q9VWR5  (Drome)

Gene ID

32857 (phm)

Ncbi ID


Available reactivities

Dros (Drosophila)

Available hosts


Available applications

Immunocytochemistry/Immunofluorescence (ICC/IF), Immunoprecipitation (IP), Western blot / Immunoblot (WB)

Background of Phantom / phm antibody

Fruit fly (Drosophila melanogaster) ovaries contains two set of germline stem cells surrounded by a group of highly differentiated somatic cells that express genes for two phenotypes (hedgehog & wingless). The TGF beta super family member, decpentaplegic (dpp) or its homologue BMP2/4 is specifically required for maintenance and promote its cell division in the female germline (1, 2). The Signaling by TGF beta-related factors requires ligand-induced association between type I and type II transmembrane receptors that have endogenous serine/threonine kinases activity. In Drosophila, the saxophone (sax) and thick veins (tkv) genes encode type I receptors that mediate signaling by decapentaplegic (dpp), a member of the bone morphogenetic protein (BMP) subgroup of TGF beta-type factors. Where as Punt and Wishful Thinking (wit) are type II receptors. Over expression or mutation in dpp suppress germline stem cell differentiation. Dpp actions are mediated by its receptor Saxophone. The Saxophone gene is expressed ubiquitously. The Saxophone gene also gives two products Brk43E and Berk25 and both gene products inter acts with TGF super family peptide ligands Dpp. Mutations that completely abolish Saxophone activity causes phenotype that are similar to partial or complete loss of activity of the dpp ligand. The saxophone products are also have serine/threonine kinase activity responsible for phsosphorylation and activation of the ligands including pMAD, Screw (Scw), and short gastrulation protein (Sog). The mutant larvae showed small synapses, defective evoke potentials and slower vesicular release and changes in the ultra-structural architect (3). Mutations in the Phantom gene disrupts the neuronal remodeling in mushroom bodies (MBs) in fruit fly (4).

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