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PIPKs are essential for rhizoid elongation and caulonemal cell development in the moss Physcomitrella patens

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Title: PIPKs are essential for rhizoid elongation and caulonemal cell development in the moss Physcomitrella patens
Authors: Saavedra, Laura Browse this author
Balbi, Virginia Browse this author
Lerche, Jennifer Browse this author
Mikami, Koji Browse this author →KAKEN DB
Heilmann, Ingo Browse this author
Sommarin, Marianne Browse this author
Keywords: Phosphatidylinositol phosphate kinase
Physcomitrella patens
Tip growth
Phosphatidylinositol (4,5) bisphosphate
Cytoskeleton organization
Issue Date: Aug-2011
Publisher: Blackwell Publishing
Journal Title: The plant journal
Volume: 67
Issue: 4
Start Page: 635
End Page: 647
Publisher DOI: 10.1111/j.1365-313X.2011.04623.x
PMID: 21554449
Abstract: PtdIns-4,5-bisphosphate is a lipid messenger of eukaryotic cells playing critical roles in processes such as cytoskeleton organization, intracellular vesicular trafficking, secretion, cell motility, regulation of ion channels and nuclear signalling pathways. The enzymes responsible for the synthesis of PtdIns(4,5)P2 are phosphatidylinositol phosphate kinases (PIPKs). The moss Physcomitrella patens contains two PIPKs, PpPIPK1 and PpPIPK2. To study their physiological role, both genes were disrupted by targeted homologous recombination and as a result mutant plants with lower PtdIns(4,5)P2 levels were obtained. A strong phenotype for pipk1, but not for pipk2 single knockout lines, was obtained. The pipk1 knockout lines were impaired in rhizoid and caulonemal cell elongation, whereas pipk1-2 double knockout lines showed dramatic defects in protonemal and gametophore morphology manifested by the absence of rapidly elongating caulonemal cells in the protonemal tissue, leafy gametophores with very short rhizoids, and loss of sporophyte production. pipk1 complemented by overexpression of PpPIPK1 fully restored the wild type phenotype whereas overexpression of the inactive PpPIPK1E885A did not. Overexpression of PpPIPK2 in the pipk1-2 double knockout did not restore the wild type phenotype demonstrating that PpPIPK1 and PpPIPK2 are not functionally redundant. In vivo imaging of the cytoskeleton network revealed that the shortened caulonemal cells in the pipk1 mutants was the result of the absence of the apicobasal gradient of cortical F-actin cables normally observed in wild type caulonemal cells. Our data indicate that both PpPIPKs play a crucial role in the development of the moss P. patens, and particularly in the regulation of tip growth.
Rights: The definitive version is available at
Type: article (author version)
Appears in Collections:水産科学院・水産科学研究院 (Graduate School of Fisheries Sciences / Faculty of Fisheries Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 三上 浩司

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