Wildlife is imperiled in peri-urban landscapes: threats to arboreal mammals.

Urbanization and deforestation impose severe challenges to wildlife, particularly for forest-living vertebrates. Understanding how the peri-urban matrix impacts their survival is critical for designing strategies to promote their conservation. We investigated the threats faced by brown howler monkeys (Alouatta guariba clamitans) in peri-urban regions of Rio Grande do Sul (RS) and Santa Catarina (SC) states, southern Brazil, by compiling negative interaction events (hereafter NIE) reported over more than two decades. We assessed the major NIEs, their distribution among age-sex classes, and the predictors of NIE-related mortality. After 20+ years of monitoring, we compiled 540 NIEs (RS = 248 and SC = 292). Electrocution by power lines was the most frequent cause of death or injury (37%), followed by dog attack (34%), vehicle collision (17%), and human mistreatment (12%). The occurrence of lethal injuries ranged from 5% to 69% depending on the type of NIE and on which state it occurred in. The overall post-NIE mortality was 56%. Adults of both sexes were the most affected individuals in both study regions. The minimal adequate GLM model explained 83% of the variation in NIE-related mortality. State, NIE type, and age-sex class were the main predictors of mortality. Overall, mortality was lower in SC and higher among adult females than in the other classes. We found that the survival of brown howler monkeys in the forest-urban interface is constrained by both the urban infrastructure and the growing interactions with humans and domestic and stray dogs (Canis familiaris). We propose the placement of aerial bridges, road signs and speed bumps in areas of frequent animal crossing, the sterilization of stray dogs, and the sensitization of local inhabitants on the importance of respecting and protecting wildlife to reduce their NIEs with humans and domestic animals in the forest-urban interface.

Complementary action of two independent dominant genes in Columbia soybean for resistance to Soybean mosaic virus.

A stem-tip necrosis disease was observed in the soybean [Glycine max (L.) Merr.] cultivar Columbia and its derivative OX686 when infected with a necrosis-causing strain of Soybean mosaic virus (SMV) in Canada. A dominant gene named Rsv3 was found in OX686 for the necrotic reaction. In the present research we have found that Columbia is resistant to all known SMV strains G1-G7, except G4. Genetic studies were conducted to investigate the inheritance of resistance in Columbia and interactions of resistance gene(s) with SMV strains. Columbia was crossed with a susceptible cultivar, Lee 68, and with resistant lines PI96983, Ogden, and LR1, each possessing a resistance gene at the Rsv1 locus. F(1) individuals, F(2) populations, and F(2:3) lines from these crosses were inoculated with G7 or G1 in the greenhouse. Our inheritance data confirmed the presence of two independent dominant genes for SMV resistance in Columbia. Results from allelism tests further demonstrate that the two genes (referred to as R3 and R4 in this article) in Columbia were independent of the Rsv1 locus. R3 appears to be the same gene previously reported as Rsv3 in OX686, which was derived from Columbia. The R3 gene confers resistance to G7, but necrosis to G1. The other gene, R4, conditions resistance to G1 and G7 at the early seedling stage and then a delayed mild mosaic reaction (late susceptible) 3 weeks later. Plants carrying both the R3 and R4 genes were completely resistant to both G1 and G7, indicating that the two genes interact in a complementary fashion. Plants heterozygous for R3 or R4 exhibited systemic necrosis or late susceptibility, suggesting that the resistance is allele dosage dependent. The R4 gene appeared epistatic to R3 since it masked expression of necrosis associated with the response of R3. The complementary interaction of two resistance genes, as exhibited in Columbia, can be useful in development of soybean cultivars with multiple and durable resistance to SMV.