Bearded sprangletop is a problematic native grass weed in California’s rice fields. The widespread and extensive use of acetyl-CoA carboxylase (ACCase)–inhibiting herbicides, such as cyhalofop-p-butyl (cyhalofop), has led to speculation that biotypes of bearded sprangletop have developed herbicide resistance to ACCase. The aim of this study was to evaluate suspected resistant bearded sprangletop biotypes, R1, R2, R3, and the susceptible biotype, S1, in terms of their levels of resistance to three ACCase-inhibiting herbicides and to characterize the molecular mechanisms of resistance. Dose–response experiments suggested that the biotype R1, R2, and R3 had high-level resistance to cyhalofop and to quizalofop-p-ethyl (quizalofop), but not clethodim. The study determined that the resistance to ACCase inhibitors was a target-site mechanism resulting from nucleotide substitution. The carboxyl transferase (CT) domain of the ACCase gene’s sequence analysis revealed the substitutions Trp-2027-Cys for R1 and R2 biotypes and Ile-2041-Asn for the R3 biotype. This study revealed the presence of target-site resistance to cyhalofop and quizalofop in at least two mutation points in representative biotypes of bearded sprangletop in California. This research highlights the significance of careful herbicide selection due to weed species responding quite rapidly to selection pressure, so as to aid in managing bearded sprangletop in rice fields.

Dilated cardiomyopathy is characterised by dilatation and impaired contraction of the left ventricle or both ventricles, which is the most common childhood cardiomyopathy. In recent years, it has been recognised that many sorts of genetic mutations may contribute to dilated cardiomyopathy. We now report a rare association of dilated cardiomyopathy with site mutation of BMPR2 gene. We did not find such an association reported in the medical literature.

The importance of various factors influencing the evolution of herbicide resistance in weeds is critically examined using population genetic models. The factors include gene mutation, initial frequency of resistance alleles, inheritance, weed fitness in the presence and absence of herbicide, mating system, and gene flow. Where weed infestations are heavy, the probability of selecting for resistance can be high even when the rate of mutation is low. Subsequent to the occurrence of a resistant mutant, repeated treatments with herbicides having the same mode of action can lead to the rapid evolution of a predominantly resistant population. At a given herbicide selection intensity, the initial frequency of resistance alleles determines the number of generations required to reach a specific frequency of resistant plants. The initial frequency of resistance alleles has a greater influence on the evolutionary process when herbicides impose weak selection, as opposed to very strong selection. Under selection, dominant resistance alleles increase in frequency more rapidly than recessive alleles in random mating or highly outcrossing weed populations. In highly self-fertilizing species, dominant and recessive resistance alleles increase in frequency at approximately the same rate. Gene flow through pollen or seed movement from resistant weed populations can provide a source of resistance alleles in previously susceptible populations. Because rates of gene flow are generally higher than rates of mutation, the time required to reach a high level of resistance in such situations is greatly reduced. Contrary to common misconception, gene flow from a susceptible population to a population undergoing resistance evolution is unlikely to slow the evolutionary process significantly. Accurate measurements of many factors that influence resistance evolution are difficult, if not impossible, to obtain experimentally. Thus, the use of models to predict times to resistance in specific situations is markedly limited. However, with appropriate assumptions, they can be invaluable in assessing the relative effectiveness of various management practices to avoid, or delay, the occurrence of herbicide resistance in weed populations.

Understanding the mechanism of herbicide resistance is fundamental for designing sustainable weed control strategies and exploiting herbicides rationally. Shortawn foxtail is a problem grass weed infesting several important crops in China. The repeated use of acetyl-CoA carboxylase (ACCase)-inhibiting herbicides has resulted in herbicide resistance in this weed. The ACCase gene of resistant individuals of a shortawn foxtail population (JSLS-1) has an Ile-2041-Thr mutation. F2 generation seeds, originated from the same heterozygous plant, were harvested, and two homozygous mutant (JSLS-1RR) and wild (JSLS-1SS) populations for the Ile-2041-Thr mutation were obtained. In whole plants, the JSLS-1RR population conferred high resistance to fenoxaprop and clodinafop, moderate resistance to haloxyfop, low resistance to pinoxaden, and no obvious resistance to clethodim and sethoxydim, compared with JSLS-1SS and a proven susceptible population (HNXY-1). A derived cleaved amplified polymorphic sequence (dCAPS) marker was developed to rapidly detect the rare Ile-2041-Thr mutation in the shortawn foxtail population. This is the first report of the cross-resistance pattern of Ile-2041-Thr mutation, and the robust dCAPS marker could quickly detect this mutation in shortawn foxtail.

We describe the case of an asymptomatic girl with sinus bradycardia and short QT interval at birth, junctional bradycardia in infancy requiring single-chamber pacemaker, atrial fibrillation in adolescence, and V141M mutation in the KCNQ1 gene. Atrial fibrillation recurred and became unresponsive to electrical or anti-arrhythmic therapy. During 20 years of follow-up, a progressive evolution from sinus node dysfunction to low-rate atrial fibrillation was observed.

We report the case of a young woman with a troponin mutation of C to T nucleotide substitution in exon 17 of troponin 2 (TNNT2; c.868C.T; p.Arg288Cys) leading to hypertrophic obstructive cardiomyopathy. Following surgical resection of the outflow obstruction, she had near-complete resolution of her asymmetric left ventricular hypertrophy, such that cardiomyopathy could no longer be diagnosed on echocardiographic grounds. We believe that this unusual case shows important aspects relating to the interplay between genetic and environmental mechanisms and the overlap in the phenotypic spectrum between primary subaortic stenosis and obstructive hypertrophic cardiomyopathy.