Differential expression of receptors for Shiga and Cholera toxin is regulated by the cell cycle
Cholera and Shiga toxin bind to the cell surface via glycolipid receptors GM1 and Gb3, respectively. Surprisingly, the majority of Vero cells from a non-synchronized population bind either Cholera or Shiga toxin but not both toxins. The hypothesis that the differential expression of toxin receptors...
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| Veröffentlicht in: | Journal of cell science 2002-02, Vol.115 (Pt 4), p.817-826 |
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| container_issue | Pt 4 |
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| container_title | Journal of cell science |
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| creator | Majoul, Irina Schmidt, Tobias Pomasanova, Maria Boutkevich, Evgenia Kozlov, Yuri Söling, Hans-Dieter |
| description | Cholera and Shiga toxin bind to the cell surface via glycolipid receptors GM1 and Gb3, respectively. Surprisingly, the majority of Vero cells from a non-synchronized population bind either Cholera or Shiga toxin but not both toxins. The hypothesis that the differential expression of toxin receptors is regulated by the cell cycle was tested. We find that Cholera toxin binds preferentially in G0/G1, with little binding through S-phase to telophase, whereas Shiga toxin binds maximally through G2 to telophase but does not bind during G0/G1 and S-phase. The changes result from the corresponding changes in Gb3 and GM1 synthesis, not from variations of receptor transport to the cell surface. The changes do not reflect competition of Gb3 and GM1 synthesis for lactosylceramide. Cells as diverse as Vero cells, PC12 cells and astrocytes show the same cell-cycle-dependent regulation of glycosphingolipid receptors, suggesting that this novel phenomenon is based on a conserved regulatory mechanism. |
| doi_str_mv | 10.1242/jcs.115.4.817 |
| format | Article |
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Surprisingly, the majority of Vero cells from a non-synchronized population bind either Cholera or Shiga toxin but not both toxins. The hypothesis that the differential expression of toxin receptors is regulated by the cell cycle was tested. We find that Cholera toxin binds preferentially in G0/G1, with little binding through S-phase to telophase, whereas Shiga toxin binds maximally through G2 to telophase but does not bind during G0/G1 and S-phase. The changes result from the corresponding changes in Gb3 and GM1 synthesis, not from variations of receptor transport to the cell surface. The changes do not reflect competition of Gb3 and GM1 synthesis for lactosylceramide. 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Surprisingly, the majority of Vero cells from a non-synchronized population bind either Cholera or Shiga toxin but not both toxins. The hypothesis that the differential expression of toxin receptors is regulated by the cell cycle was tested. We find that Cholera toxin binds preferentially in G0/G1, with little binding through S-phase to telophase, whereas Shiga toxin binds maximally through G2 to telophase but does not bind during G0/G1 and S-phase. The changes result from the corresponding changes in Gb3 and GM1 synthesis, not from variations of receptor transport to the cell surface. The changes do not reflect competition of Gb3 and GM1 synthesis for lactosylceramide. Cells as diverse as Vero cells, PC12 cells and astrocytes show the same cell-cycle-dependent regulation of glycosphingolipid receptors, suggesting that this novel phenomenon is based on a conserved regulatory mechanism.</description><subject>Animals</subject><subject>Cell Cycle</subject><subject>Cells, Cultured</subject><subject>Chlorocebus aethiops</subject><subject>G(M1) Ganglioside - biosynthesis</subject><subject>G(M1) Ganglioside - metabolism</subject><subject>G1 Phase</subject><subject>G2 Phase</subject><subject>Hippocampus - cytology</subject><subject>Mice</subject><subject>Neurons - metabolism</subject><subject>PC12 Cells</subject><subject>Rats</subject><subject>Receptors, Cell Surface - biosynthesis</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Resting Phase, Cell Cycle</subject><subject>Telophase</subject><subject>Trihexosylceramides - biosynthesis</subject><subject>Trihexosylceramides - metabolism</subject><subject>Vero Cells</subject><issn>0021-9533</issn><issn>1477-9137</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkDtPwzAYRS0EoqUwsiJPbAl-JY5HVJ5SJQZgthznc-sqjYOdSPTfk6qVWO5djq6uDkK3lOSUCfawtSmntMhFXlF5huZUSJkpyuU5mhPCaKYKzmfoKqUtIUQyJS_RjNKqLAiXc6SfvHMQoRu8aTH89hFS8qHDweEIFvohxIRdiPhz49cGm67By01oIRo8hF_fYZ8mcD22ZoAG13s8bABbaFts97aFa3ThTJvg5tQL9P3y_LV8y1Yfr-_Lx1VmBVNDpqAQxBhQgjY1qcE6YVgjpyS8IKauGkGUK0zZQE1VQZ3kylU146QUxpQlX6D7424fw88IadA7nw43TAdhTFpSUXEmqwnMjqCNIaUITvfR70zca0r0waiejOrJqBZ6Mjrxd6fhsd5B80-fFPI_F-py3w</recordid><startdate>20020215</startdate><enddate>20020215</enddate><creator>Majoul, Irina</creator><creator>Schmidt, Tobias</creator><creator>Pomasanova, Maria</creator><creator>Boutkevich, Evgenia</creator><creator>Kozlov, Yuri</creator><creator>Söling, Hans-Dieter</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20020215</creationdate><title>Differential expression of receptors for Shiga and Cholera toxin is regulated by the cell cycle</title><author>Majoul, Irina ; Schmidt, Tobias ; Pomasanova, Maria ; Boutkevich, Evgenia ; Kozlov, Yuri ; Söling, Hans-Dieter</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c429t-9e540aae941db0becf4a2d7f4a0350ab8d409f5a6deb1951f739f8b23064aa663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Cell Cycle</topic><topic>Cells, Cultured</topic><topic>Chlorocebus aethiops</topic><topic>G(M1) Ganglioside - biosynthesis</topic><topic>G(M1) Ganglioside - metabolism</topic><topic>G1 Phase</topic><topic>G2 Phase</topic><topic>Hippocampus - cytology</topic><topic>Mice</topic><topic>Neurons - metabolism</topic><topic>PC12 Cells</topic><topic>Rats</topic><topic>Receptors, Cell Surface - biosynthesis</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Resting Phase, Cell Cycle</topic><topic>Telophase</topic><topic>Trihexosylceramides - biosynthesis</topic><topic>Trihexosylceramides - metabolism</topic><topic>Vero Cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Majoul, Irina</creatorcontrib><creatorcontrib>Schmidt, Tobias</creatorcontrib><creatorcontrib>Pomasanova, Maria</creatorcontrib><creatorcontrib>Boutkevich, Evgenia</creatorcontrib><creatorcontrib>Kozlov, Yuri</creatorcontrib><creatorcontrib>Söling, Hans-Dieter</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cell science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Majoul, Irina</au><au>Schmidt, Tobias</au><au>Pomasanova, Maria</au><au>Boutkevich, Evgenia</au><au>Kozlov, Yuri</au><au>Söling, Hans-Dieter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential expression of receptors for Shiga and Cholera toxin is regulated by the cell cycle</atitle><jtitle>Journal of cell science</jtitle><addtitle>J Cell Sci</addtitle><date>2002-02-15</date><risdate>2002</risdate><volume>115</volume><issue>Pt 4</issue><spage>817</spage><epage>826</epage><pages>817-826</pages><issn>0021-9533</issn><eissn>1477-9137</eissn><abstract>Cholera and Shiga toxin bind to the cell surface via glycolipid receptors GM1 and Gb3, respectively. Surprisingly, the majority of Vero cells from a non-synchronized population bind either Cholera or Shiga toxin but not both toxins. The hypothesis that the differential expression of toxin receptors is regulated by the cell cycle was tested. We find that Cholera toxin binds preferentially in G0/G1, with little binding through S-phase to telophase, whereas Shiga toxin binds maximally through G2 to telophase but does not bind during G0/G1 and S-phase. The changes result from the corresponding changes in Gb3 and GM1 synthesis, not from variations of receptor transport to the cell surface. The changes do not reflect competition of Gb3 and GM1 synthesis for lactosylceramide. 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| ispartof | Journal of cell science, 2002-02, Vol.115 (Pt 4), p.817-826 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Company of Biologists |
| subjects | Animals Cell Cycle Cells, Cultured Chlorocebus aethiops G(M1) Ganglioside - biosynthesis G(M1) Ganglioside - metabolism G1 Phase G2 Phase Hippocampus - cytology Mice Neurons - metabolism PC12 Cells Rats Receptors, Cell Surface - biosynthesis Receptors, Cell Surface - metabolism Resting Phase, Cell Cycle Telophase Trihexosylceramides - biosynthesis Trihexosylceramides - metabolism Vero Cells |
| title | Differential expression of receptors for Shiga and Cholera toxin is regulated by the cell cycle |
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