The Membrane-Anchored BOTRYTIS-INDUCED KINASE1 Plays Distinct Roles in Arabidopsis Resistance to Necrotrophic and Biotrophic Pathogens (Record no. 41980)
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| fixed length control field | 02357nam a2200265Ia 4500 |
| 003 - CONTROL NUMBER IDENTIFIER | |
| control field | MX-MdCICY |
| 005 - DATE AND TIME OF LATEST TRANSACTION | |
| control field | 20250625124705.0 |
| 040 ## - CATALOGING SOURCE | |
| Transcribing agency | CICY |
| 090 ## - LOCALLY ASSIGNED LC-TYPE CALL NUMBER (OCLC); LOCAL CALL NUMBER (RLIN) | |
| Classification number (OCLC) (R) ; Classification number, CALL (RLIN) (NR) | B-7656 |
| 008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION | |
| fixed length control field | 250602s9999 xx |||||s2 |||| ||und|d |
| 245 10 - TITLE STATEMENT | |
| Title | The Membrane-Anchored BOTRYTIS-INDUCED KINASE1 Plays Distinct Roles in Arabidopsis Resistance to Necrotrophic and Biotrophic Pathogens |
| 490 0# - SERIES STATEMENT | |
| Volume/sequential designation | Plant Cell, 18(1), p.257-273, 2006 |
| 520 3# - SUMMARY, ETC. | |
| Summary, etc. | Plant resistance to disease is controlled by the combination of defense response pathways that are activated depending on the nature of the pathogen. We identified the Arabidopsis thaliana BOTRYTIS-INDUCED KINASE1 (BIK1)gene that is transcriptionally regulated by Botrytis cinerea infection. Inactivation of BIK1 causes severe susceptibility to necrotrophic fungal pathogens but enhances resistance to a virulent strain of the bacterial pathogen Pseudomonas syringae pv tomato. The response to an avirulent bacterial strain is unchanged, limiting the role of BIK1 to basal defense rather than race-specific resistance. The jasmonate- and ethylene-regulated defense response, generally associated with resistance to necrotrophic fungi, is attenuated in the bik1 mutant based on the expression of the plant defensin PDF1.2 gene. bik1 mutants show altered root growth, producing more and longer root hairs, demonstrating that BIK1 is also required for normal plant growth and development. Whereas the pathogen responses of bik1 are mostly dependent on salicylic acid (SA)levels, the nondefense responses are independent of SA. BIK1 is membrane-localized, suggesting possible involvement in early stages of the recognition or transduction of pathogen response. Our data suggest that BIK1 modulates the signaling of cellular factors required for defense responses to pathogen infection and normal root hair growth, linking defense response regulation with that of growth and development. |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Veronese, P. |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Nakagami, H. |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Bluhm, B. |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Abuqamar, S. |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Chen, X. |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Salmeron, J. |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Dietrich, R.A. |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Dietrich, R.A. |
| 700 12 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Mengistea, T. |
| 856 40 - ELECTRONIC LOCATION AND ACCESS | |
| Uniform Resource Identifier | <a href="https://drive.google.com/file/d/1IX2C4iwWwm1xWlo2n01A9Nom8gmIBdnK/view?usp=drivesdk">https://drive.google.com/file/d/1IX2C4iwWwm1xWlo2n01A9Nom8gmIBdnK/view?usp=drivesdk</a> |
| Public note | Para ver el documento ingresa a Google con tu cuenta: @cicy.edu.mx |
| 942 ## - ADDED ENTRY ELEMENTS (KOHA) | |
| Source of classification or shelving scheme | Clasificación local |
| Koha item type | Documentos solicitados |
| Lost status | Source of classification or shelving scheme | Damaged status | Not for loan | Collection | Home library | Current library | Shelving location | Date acquired | Total checkouts | Full call number | Date last seen | Price effective from | Koha item type |
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| Clasificación local | Ref1 | CICY | CICY | Documento préstamo interbibliotecario | 25.06.2025 | B-7656 | 25.06.2025 | 25.06.2025 | Documentos solicitados |
