Association of Phosphatidylinositol 3-Kinase with Nuclear Transcription Sites in Higher Plants

Bunney, Tom D.; Watkins, Peter A. C.; Beven, Alison F.; Shaw, Peter J.; Hernández, Luís E.; Lomonossoff, George P.; Shanks, Mike; Peart, Jan; Drobak, Bjorn K.

doi:10.2307/3871182

Cited by 27 publications

(38 citation statements)

References 10 publications

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“…TbVps34 may also act by a more indirect route. Several lines of evidence point to a role for Vps34-like enzymes in the nucleus, with suggested roles in transcription and telomere length regulation (3,63). Thus TbVps34 may have other functions in addition to its role in vesicular transport.…”

Section: Discussionmentioning

confidence: 99%

TbVps34, the Trypanosome Orthologue of Vps34, Is Required for Golgi Complex Segregation

Hall¹,

Gabernet-Castello

Voak³

et al. 2006

Journal of Biological Chemistry

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Phosphoinositides are important regulators of numerous cellular functions. The yeast class III phosphatidylinositol 3-kinase Vps34p, and its human orthologue hVPS34, are implicated in control of several key pathways, including endosome to lysosome transport, retrograde endosome to Golgi traffic, multivesicular body formation, and autophagy. We have identified the Vps34p orthologue in the African trypanosome, TbVps34. Knockdown of TbVps34 expression by RNA interference induces a severe growth defect, with a post-mitotic block to cytokinesis accompanied by a variety of morphological abnormalities. GFP2xFYVE, a chimeric protein that specifically binds phosphatidylinositol 3-phosphate, localizes to the trypanosome endosomal system and is delocalized under TbVps34 RNA interference (RNAi), confirming that TbVps34 is an authentic phosphatidylinositol 3-kinase. Expression of GFP2xFYVE enhances the TbVps34 RNAi-associated growth defect, suggesting a synthetic interaction via competition for phosphatidylinositol 3-phosphate-binding sites with endogenous FYVE domain proteins. Endocytosis of a fluid phase marker is unaffected by TbVps34 RNAi, but receptor-mediated endocytosis of transferrin and transport of concanavalin A to the lysosome are both impaired, confirming a role in membranous endocytic trafficking for TbVps34. TbVps34 knockdown inhibits export of variant surface glycoprotein, indicating a function in exocytic transport. Ultrastructural analysis revealed a highly extended Golgi apparatus following TbVps34 RNAi, whereas expression of the Golgi marker red fluorescent protein-GRASP (Grp1 (general receptor for phosphoinositides-1)-associated scaffold protein) demonstrated that trypanosomes are able to duplicate the Golgi complex but failed to complete segregation during mitosis, despite faithful replication and segregation of basal bodies and the kinetoplast. These observations implicate TbVps34 as having a role in coordinating segregation of the Golgi complex at cell division.

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Section: Discussionmentioning

confidence: 99%

TbVps34, the Trypanosome Orthologue of Vps34, Is Required for Golgi Complex Segregation

Hall¹,

Gabernet-Castello

Voak³

et al. 2006

Journal of Biological Chemistry

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“…There are three types of PI3K in animal cells (Toker and Cantly 1997). In plants, only type III PI3K has been reported (Hong and Verma 1994;Welters et al 1994;Bunney et al 2000). It has been shown that NADPH oxidase is activated by binding phosphatidylinositol 3-phosphate (PI3P), a product of PI3K, to the PX domain of p40 phox (Ellson et al 2001).…”

Section: Introductionmentioning

confidence: 98%

Phosphatidylinositol 3-phosphate is required for abscisic acid-induced hydrogen peroxide production in rice leaves

Hung

Kao

2005

Plant Growth Regul

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Rice leaves produce H 2 O 2 in response to abscisic acid (ABA), which results in induction of senescence and accumulation of NH 4 + . The upstream steps of the ABA-induced H 2 O 2 production pathway in rice leaves remain largely unclear. In animal cells, H 2 O 2 production in neutrophils is activated by phosphatidylinositol 3-phosphate (PI3P), a product of phosphatidylinositol 3-knase (PI3K). In the present study, we examined whether PI3P plays a role in H 2 O 2 production in rice leaves exposed to ABA. We found that PI3K inhibitors LY 294002 (LY) or wortmannin (WM) inhibited ABA-induced H 2 O 2 production, senescence and NH 4 + accumulation. Hydrogen peroxide almost completely rescued the inhibitory effect of LY or WM. It appears that PI3P plays a role in ABA-induced H 2 O 2 production, senescence, and NH 4 + accumulation in rice leaves.

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“…It is involved in plant growth and development, vesicle trafficking from Golgi to vacuoles and regulation of the transcriptional process (Welters et al 1994;Bunney et al 2000;Kim et al 2001). It has also been reported that extracellular Zn activates PI-3K pathway (Kim et al 2000;Eom et al 2001).…”

Section: Discussionmentioning

confidence: 96%

“…Of the different types of PI-3K reported in animals, only type III PI-3K, which makes PI3P from phosphoinositide, has been reported in plants (Bunney et al 2000). It is involved in plant growth and development, vesicle trafficking from Golgi to vacuoles and regulation of the transcriptional process (Welters et al 1994;Bunney et al 2000;Kim et al 2001).…”

Section: Discussionmentioning

confidence: 99%

Zinc-induced Cell Death in Rice (Oryza Sativa L.) Roots

2005

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Cell death in rice roots due to zinc (Zn) toxicity was investigated using inhibitors of signal molecules known to regulate programmed cell death in plants. Zn (5.0-25.0 mM) induced cell death in a dose-and timedependent manner. Sodium benzoate, a scavenger of reactive oxygen species (ROS), increased the cell viability under toxic Zn level (25.0 mM), suggesting a role of ROS in Zn-induced cell death. The protective role of rotenone in cell death indicated the involvement of mitochondrial electron transport chain in this Zn-induced ROS generation. Cantharidin and endothall, two serine/threonine phosphatase inhibitors, and sodium orthovanadate (Na 3 VO 4 ) and phenylarsine oxide (PAO), two protein tyrosine phosphatase inhibitors, blocked Zn-induced root cell death. Conversely, K252-a, a serine/threonine kinase inhibitor, increased Zn-induced cell death. Furthermore, the phosphatidylinositol 3-Kinase (PI-3K) inhibitors, LY 294002 and wortmannin inhibited Zn-induced root cell death. These results suggest that the ROS, protein phosphatase and PI-3K may function in the Zn-induced cellular toxicity in rice roots.Abbreviations: MAPK -mitogen-activated protein kinase; PAO -phenylarsine oxide; PI-3K -phosphatidylinositol 3-kinase; ROS -reactive oxygen species; SB -sodium benzoate; Na 3 VO 4 -sodium orthovanadate; Zinc -Zn

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Association of Phosphatidylinositol 3-Kinase with Nuclear Transcription Sites in Higher Plants

Cited by 27 publications

References 10 publications

TbVps34, the Trypanosome Orthologue of Vps34, Is Required for Golgi Complex Segregation

TbVps34, the Trypanosome Orthologue of Vps34, Is Required for Golgi Complex Segregation

Phosphatidylinositol 3-phosphate is required for abscisic acid-induced hydrogen peroxide production in rice leaves

Zinc-induced Cell Death in Rice (Oryza Sativa L.) Roots

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