RESUMO
Extensive use of the preemergence herbicide triallate over the last three decades has selected for resistant (R) Avena fatua L. populations in several areas of the United States and Canada. R plants are also cross-resistant to the unrelated pyrazolium herbicide difenzoquat. We made reciprocal crosses between inbred R and susceptible (S) lines to determine the genetic basis of triallate resistance. Seeds from parental lines and F(2) populations were treated with soil applications of 0.275, 0.55, or 1.1 kg/ha triallate in the greenhouse and plant heights recorded after 37 days. Surviving F(2) plants were selfed and the resulting F(3) families were screened with 1.1 kg/ha triallate. In the F(2) populations, assortment of S and R phenotypes fit a 15:1 segregation ratio, suggesting that resistance was controlled by the two independently segregating recessive genes TRR1 and TRR2. None of the 912 F(3) progeny from 51 R F(2) individuals was susceptible to triallate treatment, further supporting a two-gene mode of inheritance. There was a possible maternal effect on susceptibility at the highest triallate rate tested.
Assuntos
Avena/genética , Resistência a Medicamentos/genética , Genes Recessivos , Herbicidas/farmacologia , Trialato/farmacologia , Avena/efeitos dos fármacos , Cruzamentos Genéticos , Genes de Plantas , Pirazóis/metabolismoRESUMO
Chronic hepatic insufficiency due to anomalies of the portal venous system was diagnosed in 6 young dogs. The disorder was characterized by a variety of abnormal central nervous system signs or ascites, or both. Laboratory findings were characteristic of chronic, generalized hepatic dysfunction. The diagnosis was established by angiographic studies of the portal venous system. Of the 6 dogs, 3 died, 1 was euthanatized, and 2 are still alive and require medical management for ascites.