Gotowa bibliografia na temat „AHAS/ALS inhibitor resistance”
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Artykuły w czasopismach na temat "AHAS/ALS inhibitor resistance"
Gerwick, B. Clifford, Linda C. Mireles i Robert J. Eilers. "Rapid Diagnosis of Als/Ahas-Resistant Weeds". Weed Technology 7, nr 2 (czerwiec 1993): 519–24. http://dx.doi.org/10.1017/s0890037x00027986.
Pełny tekst źródłaLebaron, Homer M. "Weed Science in the 1990s: Will It be Forward or in Reverse?" Weed Technology 4, nr 3 (wrzesień 1990): 671–89. http://dx.doi.org/10.1017/s0890037x00026208.
Pełny tekst źródłaYu, Qin, i Stephen B. Powles. "Resistance to AHAS inhibitor herbicides: current understanding". Pest Management Science 70, nr 9 (20.01.2014): 1340–50. http://dx.doi.org/10.1002/ps.3710.
Pełny tekst źródłaNorazua, Zakaria, Ahmad-Hamdani Muhammad Saiful i Juraimi Abdul Shukor. "Patterns of resistance to AHAS inhibitors in Limnocharis flava from Malaysia". Plant Protection Science 54, No. 1 (24.11.2017): 48–59. http://dx.doi.org/10.17221/131/2016-pps.
Pełny tekst źródłaRodriguez, Jeanette, Amber Hauvermale, Arron Carter, Rachel Zuger i Ian C. Burke. "An ALA 122 THR substitution in the AHAS / ALS gene confers imazamox‐resistance in Aegilops cylindrica". Pest Management Science 77, nr 10 (25.06.2021): 4583–92. http://dx.doi.org/10.1002/ps.6498.
Pełny tekst źródłaEberlein, Charlotte V., Mary J. Guttieri, Philip H. Berger, John K. Fellman, Carol A. Mallory-Smith, Donn C. Thill, Roger J. Baerg i William R. Belknap. "Physiological consequences of mutation for ALS-inhibitor resistance". Weed Science 47, nr 4 (sierpień 1999): 383–92. http://dx.doi.org/10.1017/s0043174500091967.
Pełny tekst źródłaBeckie, Hugh J., i Xavier Reboud. "Selecting for Weed Resistance: Herbicide Rotation and Mixture". Weed Technology 23, nr 3 (wrzesień 2009): 363–70. http://dx.doi.org/10.1614/wt-09-008.1.
Pełny tekst źródłaBeckie, H. J., L. M. Hall, F. J. Tardif i G. Séguin-Swartz. "Acetolactate synthase inhibitor-resistant stinkweed (Thlaspi arvense L.) in Alberta". Canadian Journal of Plant Science 87, nr 4 (1.10.2007): 965–72. http://dx.doi.org/10.4141/cjps06019.
Pełny tekst źródłaShergill, Lovreet S., Jenna Malone, Peter Boutsalis, Christopher Preston i Gurjeet Gill. "Basis of ACCase and ALS inhibitor resistance inHordeum glaucumSteud". Pest Management Science 73, nr 8 (15.02.2017): 1638–47. http://dx.doi.org/10.1002/ps.4501.
Pełny tekst źródłaOsuna, M. D., i R. De Prado. "Conyza albida : a new biotype with ALS inhibitor resistance". Weed Research 43, nr 3 (9.05.2003): 221–26. http://dx.doi.org/10.1046/j.1365-3180.2003.00337.x.
Pełny tekst źródłaRozprawy doktorskie na temat "AHAS/ALS inhibitor resistance"
Friesen, Lincoln Jacob Shane. "Identification of the mechanisms of wild radish herbicide resistance to PSII inhibitors, auxinics, and AHAS inhibitors". University of Western Australia. School of Plant Biology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0106.
Pełny tekst źródłaFerguson, Gabrielle Mary. "ALS-inhibitor resistance in populations of Amaranthus powellii S. Wats. and Amaranthus retroflexus L". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0023/MQ51062.pdf.
Pełny tekst źródłaIwakami, Satoshi. "Molecular mechanism of resistance in a multiple-herbicide resistant Echinochloa phyllopogon". Kyoto University, 2013. http://hdl.handle.net/2433/180368.
Pełny tekst źródła0048
新制・課程博士
博士(農学)
甲第17830号
農博第2015号
新制||農||1016(附属図書館)
学位論文||H25||N4787(農学部図書室)
30645
京都大学大学院農学研究科農学専攻
(主査)教授 稲村 達也, 教授 冨永 達, 教授 奥本 裕
学位規則第4条第1項該当
Weerasooriya, Dilooshi Kumari. "Genetic analysis of interveinal chlorosis and reduced seedling vigor as related to agronomic performance in sorghum resistant to ALS inhibitor herbicides". Diss., Kansas State University, 2016. http://hdl.handle.net/2097/32896.
Pełny tekst źródłaDepartment of Agronomy
Tesfaye T. Tesso
The lack of effective post-emergence weed control options is often highlighted as one of the major factors behind dwindling acreage under sorghum (Sorghum bicolor (L.) Moench) in the United States. The discovery of herbicide resistance sources in wild sorghum population and subsequent efforts to incorporate them into cultivated sorghum was received with much optimism to change weed management practices in sorghum. As the development of the technology advances, especially of the Acetolactate synthase (ALS) resistance, concerns over the temporary interveinal chlorosis and reduced seedling vigor in some of the resistant families became heightened. This thesis research is designed to shed light on the genetic basis of seedling chlorosis and assess its impacts on yield potential. The study has three parts; the first part is focused on identifying the genetic causes and plant mechanisms associated with the chlorotic phenotype. ALS herbicide resistant sister-lines expressing normal and chlorotic phenotypes were analyzed via RNA sequencing at four time points during seedling growth. The study identified several variants of genes coding chloroplast precursors and those that cause epigenetic modifications. Once confirmed, genetic markers can be developed to track these gene variants in the breeding population and eliminate segregates genetically prone to chlorosis/yellowing. The second part of the study focuses on assessing the effect of ALS resistance associated chlorosis on agronomic and nutritional parameters of sorghum inbred lines. A set of ALS resistant lines expressing different levels of the chlorotic phenotype were evaluated in replicated field trials and laboratory methods. Results showed that interveinal chlorosis delays flowering but does not have negative effect on yield and nutritional parameters with and without herbicide treatment. The last part addresses whether there is any yield drag that may be associated with herbicide resistance traits and foliar interveinal chlorosis. For this, we synthesized a large set (182) of hybrids from ALS resistant, ACCase resistant and regular (susceptible) seed and pollinator parents. The hybrids were then evaluated in three sets at multiple locations during the 2014 and 2015 crop seasons along with commercial checks. The results revealed that resistance to both herbicides do not cause any drag to grain yield. The traits also do not have any negative impact on grain and nutritional quality of resistant hybrids.
Kershner, Kellan Scott. "Herbicide resistance in grain sorghum". Diss., Kansas State University, 2010. http://hdl.handle.net/2097/13069.
Pełny tekst źródłaDepartment of Agronomy
Kassim Al-Khatib
Mitchell R. Tuinstra
Sorghum acreage is declining throughout the United States because management options and yield have not maintained pace with maize improvements. The most extreme difference has been the absence of herbicide technology development for sorghum over the past twenty years. The objectives of this study were to evaluate the level of resistance, type of inheritance, and causal mutation of wild sorghums that are resistant to either acetyl-coenzyme A carboxylase (ACCase)-inhibiting herbicides or acetohydroxyacid synthase (AHAS)-inhibiting herbicides. ACCase-inhibiting herbicides used in this study were aryloxyphenoxypropionate (APP) family members fluazifop-P and quizalofop-P along with cyclohexanedione (CHD) family members clethodim and sethoxydim. The level of resistance was very high for APP herbicides but low to nonexistent to CHD herbicides. With genetic resistance to APP herbicides, the resistance factors, the ratio of resistance to susceptible, were greater than 54 to 64 for homozygous individuals and greater than 9 to 20 for heterozygous individuals. Resistance to CHD herbicides was very low with resistance factors ranging from one to about five. Genetic segregation studies indicate a single gene is the cause of resistance to APP herbicides. Sequencing identified a single mutation that results in cysteine replacing tryptophan (Trp-2027-Cys). Trp-2027-Cys has previously been reported to provide resistance to APP but not CHD herbicides. The other wild sorghum evaluated in this study was resistant to AHAS-inhibiting herbicides including imidazolinone (IM) family member, imazapyr, and sulfonylurea (SU) family member, nicosulfuron. Resistance factors in this genotype were very high, greater than 770 for the IM herbicide and greater than 500 for the SU herbicide, for both herbicide chemical families. Genetic segregation studies demonstrate that resistance was controlled by one major locus and two modifier loci. DNA sequencing of the AHAS gene identified two mutations, Val-560-Ile and Trp-574-Leu. Val-560-Ile is of unknown importance, but valine and isoleucine are similar and residue 560 is not conserved. Trp-574 is a conserved residue and Leu-574 is a known mutation that provides strong cross resistance to IM and SU herbicides. The results of these studies suggest that these sources of APP, SU, and IM resistance may provide useful herbicide resistance traits for use in sorghum.
Park, Kee-Woong. "ALS-inhibitor resistant downy brome (Bromus tectorum L.) biotypes in Oregon : mechanism of resistance, fitness, and competition". Thesis, 2003. http://hdl.handle.net/1957/30435.
Pełny tekst źródłaCzęści książek na temat "AHAS/ALS inhibitor resistance"
Eberlein, C. V., M. J. Guttieri, C. A. Mallory-Smith i D. C. Thill. "Effects of Mutation for ALS-Inhibitor Resistance on ALS Activity in Resistant and Susceptible Near-Isonuclear Lactuca Lines". W Weed and Crop Resistance to Herbicides, 191–97. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5538-0_21.
Pełny tekst źródłaStreszczenia konferencji na temat "AHAS/ALS inhibitor resistance"
Ouyang, Xiaoming, Ashley Barling, Aletha Lesch, Jeffrey Tyner, Sophia Jeng, Christina Zheng, Sara A. Courtneidge, Shannon McWeeney i Molly Kulesz-Martin. "Abstract 78: Inhibiting anaplastic lymphoma kinase (ALK) overcomes epidermal growth factor receptor (EGFR) inhibitor resistance in head and neck squamous cell carcinoma (HNSCC) patient-derived models". W Abstracts: AACR-AHNS Head and Neck Cancer Conference: Optimizing Survival and Quality of Life through Basic, Clinical, and Translational Research; April 23-25, 2017; San Diego, CA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3265.aacrahns17-78.
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