MARC details
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02887nam a2200265Ia 4500 |
| 003 - CONTROL NUMBER IDENTIFIER |
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MX-MdCICY |
| 005 - DATE AND TIME OF LATEST TRANSACTION |
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20250625140632.0 |
| 040 ## - CATALOGING SOURCE |
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| Transcribing agency |
CICY |
| 090 ## - LOCALLY ASSIGNED LC-TYPE CALL NUMBER (OCLC); LOCAL CALL NUMBER (RLIN) |
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| Classification number (OCLC) (R) ; Classification number, CALL (RLIN) (NR) |
B-10449 |
| 008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION |
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250602s9999 xx |||||s2 |||| ||und|d |
| 245 10 - TITLE STATEMENT |
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| Title |
Two distinct intracellular Ca2+-release components act in opposite ways in the regulation of the auxin-dependent MIA biosynthesis in Catharanthus roseus cells |
| 490 0# - SERIES STATEMENT |
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| Volume/sequential designation |
Journal of Experimental Botany, 60, p.1387-1398, 2009 |
| 520 3# - SUMMARY, ETC. |
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| Summary, etc. |
Calcium-mediated signalling is ubiquitous in both animals and plants. Changes in cytoplasmic free Ca2+ concentration couple diverse arrays of stimuli to their specific responses, the specificity of the stimulus being determined by integrated actions between multiple Ca2+ mobilization pathways. In this work, a pharmacological approach is reported, aimed at deciphering the role of calcium as a second messenger in the transduction pathway leading to the inhibitory effect of 2,4-dichlorophenoxyacetic acid (2,4-D), in regulating monoterpene indole alkaloid (MIA)biosynthesis in Catharanthus roseus cells. It is demonstrated here that auxin-dependent MIA biosynthesis is differentially regulated by two distinct calcium release components from internal stores in C. roseus showing pharmacological profiles similar to those displayed by animal RyR and IP3 channels. MIA biosynthesis is stimulated by caffeine (Ca2+-release activator through RyR channels)and by heparin and TMB8 (Ca2+-release inhibitors of IP3 channels)whereas MIA biosynthesis is inhibited by mastoparan (Ca2+-release activator of IP3 channels)and by ruthenium red and DHBP (Ca2+-release inhibitors of RyR channels). Furthermore, calcium, as 2,4-D, acts on MIA biosynthesis by regulating the monoterpene moiety of the MIA biosynthesis pathway since calcium channel modulators preferentially modulate g10h expression, the gene encoding the enzyme of the secoiridoid monoterpene pathway, that is the major target of 2,4-D action. In addition, the simultaneous use of caffeine (an activator of RyR channel in animals)and TMB8 (an inhibitor of the IP3 channel)in 2,4-D treated cells triggers a synergistic effect on MIA accumulation. This finding suggests an opposite and co-ordinated action of multiple Ca2+-release pathways in 2,4-D signal transduction, adding a new level of complexity to calcium signalling in plants and questioning the existence of RyR and IP3 channels in plants. |
| 650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM |
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| Topical term or geographic name entry element |
2,4-D |
| 650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM |
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| Topical term or geographic name entry element |
CALCIUM SIGNALLING |
| 650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM |
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| Topical term or geographic name entry element |
CATHARANTHUS ROSEUS |
| 650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM |
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| Topical term or geographic name entry element |
MONOTERPENOID INDOLE ALKALOID |
| 700 12 - ADDED ENTRY--PERSONAL NAME |
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| Personal name |
Poutrain, P. |
| 700 12 - ADDED ENTRY--PERSONAL NAME |
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| Personal name |
Mazars, C. |
| 700 12 - ADDED ENTRY--PERSONAL NAME |
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| Personal name |
Thiersault, M. |
| 700 12 - ADDED ENTRY--PERSONAL NAME |
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| Personal name |
Rideau, M. |
| 700 12 - ADDED ENTRY--PERSONAL NAME |
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| Personal name |
Pichon, O. |
| 856 40 - ELECTRONIC LOCATION AND ACCESS |
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| Uniform Resource Identifier |
<a href="https://drive.google.com/file/d/1U_va1XhJVgQXH5_hxTeSPITg1yDW9d8v/view?usp=drivesdk">https://drive.google.com/file/d/1U_va1XhJVgQXH5_hxTeSPITg1yDW9d8v/view?usp=drivesdk</a> |
| Public note |
Para ver el documento ingresa a Google con tu cuenta: @cicy.edu.mx |
| 942 ## - ADDED ENTRY ELEMENTS (KOHA) |
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| Source of classification or shelving scheme |
Clasificación local |
| Koha item type |
Documentos solicitados |
