Resistance to ACCase-inhibiting herbicides in sprangletop (Leptochloa chinensis)

This study reports evolved resistance to fenoxaprop-P in a population of sprangletop from a rice field in Thailand (BLC1). After eight applications of fenoxaprop-P, the herbicide appeared no longer effective. To confirm herbicide resistance in the BLC1 population, three experiments were conducted. First, glasshouse experiments revealed that the BLC1 population survived 600 g ai ha-1 of fenoxaprop-P without visual injury. Second, the BLC1 population was treated with fenoxaprop-P and other acetyl coenzyme A carboxylase (ACCase)-inhibiting herbicides (quizalofop-P, cyhalofopbutyl, and profoxydim) under field conditions; BLC1 exhibited resistance to all of these herbicides. Third, seeds of susceptible SLC1 and resistant BLC1 were germinated on 0.6% (v/v) agar across a range of herbicide concentrations. The resistant BLC1 population exhibited 61-, 44-, 9- and 8-fold resistance to fenoxaprop-P, cyhalofop, quizalofop-P, and profoxydim, respectively, compared with a susceptible SLC1 population. At the enzyme level, ACCase from the resistant BLC1 exhibited 30, 24, 11, 4, and 5 times resistance to fenoxaprop, cyhalofop-butyl, haloxyfop, clethodim, and cycloxydim, respectively. The spectrum of resistance at the whole plant level correlated well with resistance at the ACCase level. Hence, the mechanism of resistance to ACCase-inhibiting herbicides in this biotype of sprangletop is a herbicide-resistant ACCase. The specific mutation(s) of the ACCase gene that endows resistance in this population remains to be investigated

Herbicide resistance-endowing ACCase gene mutations in hexaploid wild oat (Avena fatua): insights into resistance evolution in a hexaploid species

Many herbicide-resistant weed species are polyploids, but far too little about the evolution of resistance mutations in polyploids is understood. Hexaploid wild oat (Avena fatua) is a global crop weed and many populations have evolved herbicide resistance. We studied plastidic acetyl-coenzyme A carboxylase (ACCase)-inhibiting herbicide resistance in hexaploid wild oat and revealed that resistant individuals can express one, two or three different plastidic ACCase gene resistance mutations (Ile-1781-Leu, Asp-2078-Gly and Cys-2088-Arg). Using ACCase resistance mutations as molecular markers, combined with genetic, molecular and biochemical approaches, we found in individual resistant wild-oat plants that (1) up to three unlinked ACCase gene loci assort independently following Mendelian laws for disomic inheritance, (2) all three of these homoeologous ACCase genes were transcribed, with each able to carry its own mutation and (3) in a hexaploid background, each individual ACCase resistance mutation confers relatively low-level herbicide resistance, in contrast to high-level resistance conferred by the same mutations in unrelated diploid weed species of the Poaceae (grass) family. Low resistance conferred by individual ACCase resistance mutations is likely due to a dilution effect by susceptible ACCase expressed by homoeologs in hexaploid wild oat and/or differential expression of homoeologous ACCase gene copies. Thus, polyploidy in hexaploid wild oat may slow resistance evolution. Evidence of coexisting non-target-site resistance mechanisms among wild-oat populations was also revealed. In all, these results demonstrate that herbicide resistance and its evolution can be more complex in hexaploid wild oat than in unrelated diploid grass weeds. Our data provide a starting point for the daunting task of understanding resistance evolution in polyploids

Recent Advances in Mitochondrial Fission/Fusion-Targeted Therapy in Doxorubicin-Induced Cardiotoxicity

Doxorubicin (DOX) has been recognized as one of the most effective chemotherapies and extensively used in the clinical settings of human cancer. However, DOX-mediated cardiotoxicity is known to compromise the clinical effectiveness of chemotherapy, resulting in cardiomyopathy and heart failure. Recently, accumulation of dysfunctional mitochondria via alteration of the mitochondrial fission/fusion dynamic processes has been identified as a potential mechanism underlying DOX cardiotoxicity. DOX-induced excessive fission in conjunction with impaired fusion could severely promote mitochondrial fragmentation and cardiomyocyte death, while modulation of mitochondrial dynamic proteins using either fission inhibitors (e.g., Mdivi-1) or fusion promoters (e.g., M1) can provide cardioprotection against DOX-induced cardiotoxicity. In this review, we focus particularly on the roles of mitochondrial dynamic pathways and the current advanced therapies in mitochondrial dynamics-targeted anti-cardiotoxicity of DOX. This review summarizes all the novel insights into the development of anti-cardiotoxic effects of DOX via the targeting of mitochondrial dynamic pathways, thereby encouraging and guiding future clinical investigations to focus on the potential application of mitochondrial dynamic modulators in the setting of DOX-induced cardiotoxicity