A cytochrome P450 monooxygenase commonly used for negative selection in transgenic plants causes growth anomalies by disrupting brassinosteroid signaling

التفاصيل البيبلوغرافية
العنوان: A cytochrome P450 monooxygenase commonly used for negative selection in transgenic plants causes growth anomalies by disrupting brassinosteroid signaling
المؤلفون: Brian G. Ayre, Sindhu Manivasagam, Savita Ganesan, Kasturi Dasgupta
المصدر: BMC Plant Biology, Vol 11, Iss 1, p 67 (2011)
BMC Plant Biology
بيانات النشر: Springer Science and Business Media LLC, 2011.
سنة النشر: 2011
مصطلحات موضوعية: 0106 biological sciences, Transgene, Mutant, Arabidopsis, Plant Science, 01 natural sciences, 03 medical and health sciences, chemistry.chemical_compound, Negative selection, Bacterial Proteins, Cytochrome P-450 Enzyme System, Plant Growth Regulators, lcsh:Botany, Brassinosteroid, Gene, 030304 developmental biology, 2. Zero hunger, Genetics, 0303 health sciences, biology, food and beverages, Cytochrome P450, Monooxygenase, Plants, Genetically Modified, biology.organism_classification, Streptomyces, lcsh:QK1-989, chemistry, biology.protein, Genetic Engineering, Research Article, Signal Transduction, 010606 plant biology & botany
الوصف: Background Cytochrome P450 monooxygenases form a large superfamily of enzymes that catalyze diverse reactions. The P450 SU1 gene from the soil bacteria Streptomyces griseolus encodes CYP105A1 which acts on various substrates including sulfonylurea herbicides, vitamin D, coumarins, and based on the work presented here, brassinosteroids. P450 SU1 is used as a negative-selection marker in plants because CYP105A1 converts the relatively benign sulfonyl urea pro-herbicide R7402 into a highly phytotoxic product. Consistent with its use for negative selection, transgenic Arabidopsis plants were generated with P450 SU1 situated between recognition sequences for FLP recombinase from yeast to select for recombinase-mediated excision. However, unexpected and prominent developmental aberrations resembling those described for mutants defective in brassinosteroid signaling were observed in many of the lines. Results The phenotypes of the most affected lines included severe stunting, leaf curling, darkened leaves characteristic of anthocyanin accumulation, delayed transition to flowering, low pollen and seed yields, and delayed senescence. Phenotype severity correlated with P450 SU1 transcript abundance, but not with transcript abundance of other experimental genes, strongly implicating CYP105A1 as responsible for the defects. Germination and seedling growth of transgenic and control lines in the presence and absence of 24-epibrassinolide indicated that CYP105A1 disrupts brassinosteroid signaling, most likely by inactivating brassinosteroids. Conclusions Despite prior use of this gene as a genetic tool, deleterious growth in the absence of R7402 has not been elaborated. We show that this gene can cause aberrant growth by disrupting brassinosteroid signaling and affecting homeostasis.
تدمد: 1471-2229
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::71fca6b66de4e619d53505371d373537
https://doi.org/10.1186/1471-2229-11-67
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....71fca6b66de4e619d53505371d373537
قاعدة البيانات: OpenAIRE