Resistência de buva aos herbicidas auxinicos: identificação dos biótipos, caracterização do mecanismo de resistência e controle alternativo

Abstract

Weed resistance is a worldwise problem, which are getting importance in Brazil in the last years. The plants belonging to the genus Conyza are one of the main weeds in Brazil, due to the resistance to various herbicides and its aggressivity. The objectives of this work were: to identify Conyza spp. biotypes resistant to auxinic herbicides; to verify if enhancement degradation is the mechanism of resistance responsible for the biotype resistance and find alternative herbicides to control the resistant plants. To achieve the aims, three different trials were conducted. The first one consisted of six biotypes submitted to a dose-response experiment with the herbicides 2,4-D, dicamba, triclopyr and Florpyrauxifen-benzil. The biotype 206 was susceptible to all herbicides, and it was used as parameter of comparison with the others. The biotypes 17 and 194 showed resistance to all four herbicides studied. The biotypes 35 and 108 only to 2,4-D, and the 28 to 2,4-D and dicamba. To identify if the resistance was by enhancement degradation, the biotypes were submitted to doses-response with and without acephate, a compound that inhibit the cytochrome P450 monooxygenases enzymes. Only biotype 28 for the 2,4-D herbicide showed lower doses to control 50% of its population with acephate, indicating that the enhancement degradation could be related to this biotype resistance. But, despised the difference, the biotype 28 continued to meet the criteria to be considered resistant, even with the used of acephate. The third part consisted in three trials to find alternative controls to the resistant biotypes. Different mixtures with glufosinate plus herbicides inhibitors of PROTOX enzymes were used in the first one. In the second, 2,4-D was applied in all treatments followed by different sequential ten days after. The third trial was a two factorial arrangement where the Factor A was composed of different auxinic herbicides and the Factor B was the presence or the absence of glufosinate applied 10 days after the Factor A. In the control alternative experiment, all mixtures with glufosinate plus PROTOX inhibitors were efficient controlling the plants, likewise the sequential application with glufosinate ten days after different auxinic herbicides. Satisfactory controls were observed with the application of different herbicides ten days after 2,4-D too, with controls greater than 90% in most of the treatments. The biotypes showed resistance to at least one of the four auxinic herbicides tested and the enhancement degradation by cytochrome P450 monooxygenases enzymes is not responsible for the resistance. The biotypes control can be done with glufosinate plus PROTOX inhibitors herbicides or with the sequential application of contact herbicides ten days after auxinic herbicides.