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Two cyanobacterial morphotypes isolated from Signy Island, South Orkney Islands, maritime Antarctica were characterised using a polyphasic approach combining morphological, cytological and molecular analyses. These analyses showed that the strains grouped with members of the genus Wilmottia. This genus currently includes three species, W. murrayi, W. stricta, and W. koreana. Both morphotypes analysed in this study were placed within the clade of W. murrayi. This clade showed a well-supported separation from Antarctic and New Zealand strains, as well as strains from other regions. W. murrayi was first described from Antarctica and is now known from several Antarctic regions. Confirmation of the occurrence of W. murrayi at Signy Island significantly extends its known distribution in Antarctica. In addition, a new combination, W. arthurensis, is suggested for Phormidium arthurensis.
<P>Retrograde bone morphogenetic protein signaling mediated by the Glass bottom boat (Gbb) ligand modulates structural and functional synaptogenesis at the <I>Drosophila melanogaster</I> neuromuscular junction. However, the molecular mechanisms regulating postsynaptic Gbb release are poorly understood. In this study, we show that <I>Drosophila</I> Rich (dRich), a conserved Cdc42-selective guanosine triphosphatase–activating protein (GAP), inhibits the Cdc42–Wsp pathway to stimulate postsynaptic Gbb release. Loss of dRich causes synaptic undergrowth and strongly impairs neurotransmitter release. These presynaptic defects are rescued by targeted postsynaptic expression of wild-type dRich but not a GAP-deficient mutant. dRich inhibits the postsynaptic localization of the Cdc42 effector Wsp (<I>Drosophila</I> orthologue of mammalian Wiskott-Aldrich syndrome protein, WASp), and manifestation of synaptogenesis defects in <I>drich</I> mutants requires Wsp signaling. In addition, dRich regulates postsynaptic organization independently of Cdc42. Importantly, dRich increases Gbb release and elevates presynaptic phosphorylated Mad levels. We propose that dRich coordinates the Gbb-dependent modulation of synaptic growth and function with postsynaptic development.</P>