Biochemical and biological functions of class I phosphatidylinositol transfer proteins

Cockcroft, Shamshad; Carvou, Nicolas

doi:10.1016/j.bbalip.2007.03.009

Cited by 79 publications

(65 citation statements)

References 86 publications

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“…In addition, PITPa was identified as a reconstitution factor in a cell-free assay designed to re-establish cis-to-medial intra-Golgi vesicular transport (Paul et al, 1998), and as a vesiculating factor for the scission of coatomer-coated vesicles (Simon et al, 1998). In all of these studies, either PITPa or PITPb were functional in the reconstitution assays and moreover, the yeast PITP, Sec14p, which bears no structural or sequence similarity to mammalian PITPs, could also be used (Phillips et al, 2006b;Cockcroft and Carvou, 2007). In yeast, Sec14p is required for vesicular transport from the Golgi to the plasma membrane and it is thought that it controls diacylglycerol levels, which in turn regulate vesicular transport (Howe and McMaster, 2006).…”

Section: Introductionmentioning

confidence: 99%

Phosphatidylinositol- and phosphatidylcholine-transfer activity of PITPβ is essential for COPI-mediated retrograde transport from the Golgi to the endoplasmic reticulum

Carvou

Holic̆

et al. 2010

Journal of Cell Science

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SummaryVesicles formed by the COPI complex function in retrograde transport from the Golgi to the endoplasmic reticulum (ER). Phosphatidylinositol transfer protein b (PITPb), an essential protein that possesses phosphatidylinositol (PtdIns) and phosphatidylcholine (PtdCho) lipid transfer activity is known to localise to the Golgi and ER but its role in these membrane systems is not clear. To examine the function of PITPb at the Golgi-ER interface, RNA interference (RNAi) was used to knockdown PITPb protein expression in HeLa cells. Depletion of PITPb leads to a decrease in PtdIns(4)P levels, compaction of the Golgi complex and protection from brefeldin-Amediated dispersal to the ER. Using specific transport assays, we show that anterograde traffic is unaffected but that KDEL-receptordependent retrograde traffic is inhibited. This phenotype can be rescued by expression of wild-type PITPb but not by mutants defective in docking, PtdIns transfer and PtdCho transfer. These data demonstrate that the PtdIns and PtdCho exchange activity of PITPb is essential for COPI-mediated retrograde transport from the Golgi to the ER.

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Section: Introductionmentioning

confidence: 99%

Phosphatidylinositol- and phosphatidylcholine-transfer activity of PITPβ is essential for COPI-mediated retrograde transport from the Golgi to the endoplasmic reticulum

Carvou

Holic̆

et al. 2010

Journal of Cell Science

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“…By inverse PCR on genomic DNA from pe1209 animals and sequencing (15), we identified a Mos1 insertion into a previously uncharacterized gene M01F1.7, which encodes an ortholog of class IIA PITPs conserved among vertebrates and invertebrates (Fig. 1C) (16). We hereafter refer to this gene as pitp-1.…”

Section: Resultsmentioning

confidence: 99%

“…Class IIA PITPs are multidomain proteins with an N-terminal PITP domain, a central DDHD domain implicated in metal binding, and a C-terminal LNS2 domain of unknown function (Fig. 1D) (16). Previous studies in Drosophila have shown that mutations in the class IIA PITP, retinal degeneration B (rdgB), cause light-dependent photoreceptor degeneration (17,18).…”

Section: Resultsmentioning

confidence: 99%

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Roles for class IIA phosphatidylinositol transfer protein in neurotransmission and behavioral plasticity at the sensory neuron synapses of Caenorhabditis elegans

Iwata

Oda²,

Kunitomo³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Growing evidence suggests that sensory neuron synapses not merely pass, but actively encode sensory information and convey it to the central nervous system. The chemosensory preferences of Caenorhabditis elegans, as manifested in the direction of chemotaxis, are reversibly regulated by prior experience at the level of sensory neurons; the attractive drive is promoted by diacylglycerol (DAG) signaling, whereas the counteracting repulsive drive requires PtdIns(3,4,5)P 3 signaling. Here we report that the two opposing drives require a class IIA phosphatidylinositol transfer protein (PITP), PITP-1, which localizes to the sensory neuron synapses. In pitp-1 mutants, attraction behavior to salt is reduced, whereas conditioned repulsion from salt is eliminated: the mutants inflexibly show weak attraction behavior to salt, irrespective of prior experience. To generate flexible behavioral outputs, attraction and repulsion, PITP-1 acts in the gustatory neuron ASER and likely regulates neurotransmission from ASER, as pitp-1 mutations do not affect the ASER Ca 2+ response to sensory stimulus. Furthermore, full attraction to salt is restored in pitp-1 mutants by expression of the phosphatidylinositol transfer domain alone, and also by mutations of a DGK gene that cause accumulation of DAG, suggesting that PITP-1 serves for DAG production via phosphatidylinositol transport and, hence, regulates synaptic transmission. In addition to gustatory behavior, olfactory behaviors and osmotic avoidance are also regulated by PITP-1 in the sensory neurons that detect each sensory stimulus. Thus, PITP-1-dependent phosphatidylinositol transport is essential for sensory neuron synapses to couple sensory inputs to effective behavioral responses.T he sensory information detected by the peripheral neurons is represented as a topographic neural map in the mammalian brain (1). In contrast, in the relatively simple nervous system of invertebrates devoid of extensive neural maps, much of the information processing occurs at the level of local sensory circuits, or in extreme cases, sensory neurons themselves (2-5). The fewer connections between sensory and motor neurons demand the processing at the sensory neuron level be more dominant. In the neural circuit of Aplysia gill-withdrawal reflex, for example, mechanosensory neurons innervating the siphon make direct connections with gill motorneurons. Presynaptic facilitation is caused at the synapses by aversive conditioning that induces short-and long-term memory (3).Consisting of only 302 neurons, the nervous system of the nematode Caenorhabditis elegans is even more compact (6). Despite being quite compact, C. elegans displays a rich repertoire of sensory behaviors, and moreover, each behavior is plastic and changes with experience (7). A complete reversal in behavior is observed when worms are starved in the presence of NaCl, which is normally an attractive taste. Animals previously soaked in NaCl-containing buffer without food show avoidance behavior against NaCl instead of attraction (8). The swi...

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“…This activity is found in all eukaryotic cells examined and is essential for sustained lipid signaling, intracellular trafficking, and other membrane transactions (Phillips et al 2006b;Cockcroft and Carvou 2007). Functional PITPs include small soluble proteins, represented by PITPa and PITPb in mammals (class I); a homologous subfamily of larger, membrane-spanning proteins typified by the Drosophila retinal-degeneration B (RdgB) protein (class II); and a nonhomologous group related to yeast Sec14p (class III).…”

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confidence: 99%

Modifier Genes for Mouse Phosphatidylinositol Transfer Protein α (vibrator) That Bypass Juvenile Lethality

Concepcion

Johannes

et al. 2011

Genetics

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Phosphatidylinositol transfer proteins (PITPs) mediate lipid signaling and membrane trafficking in eukaryotic cells. Loss-of-function mutations of the gene encoding PITPa in mice result in a range of dosagesensitive phenotypes, including neurological dysfunction, neurodegeneration, and premature death. We have previously reported genetic suppression of a strong hypomorphic allele, vibrator, by a wild-derived variant of Nxf1, which increases the level of PITPa made from vibrator alleles and suppresses each of the neurological and survival phenotypes. Here we report discovery and genetic mapping of additional vibrator modifiers, Mvb2 and Mvb3, from a different strain background that suppresses juvenile lethality without suppressing visible phenotypes or gene expression. Genotype-specific survival analysis predicts molecular heterosis at Mvb3. These results indicate a mechanism of suppression that bypasses a quantitative requirement for PITPa function.

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Biochemical and biological functions of class I phosphatidylinositol transfer proteins

Cited by 79 publications

References 86 publications

Phosphatidylinositol- and phosphatidylcholine-transfer activity of PITPβ is essential for COPI-mediated retrograde transport from the Golgi to the endoplasmic reticulum

Phosphatidylinositol- and phosphatidylcholine-transfer activity of PITPβ is essential for COPI-mediated retrograde transport from the Golgi to the endoplasmic reticulum

Roles for class IIA phosphatidylinositol transfer protein in neurotransmission and behavioral plasticity at the sensory neuron synapses of Caenorhabditis elegans

Modifier Genes for Mouse Phosphatidylinositol Transfer Protein α (vibrator) That Bypass Juvenile Lethality

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