Universidade Federal de Viçosa

About: Universidade Federal de Viçosa is a education organization based out in Viçosa, Brazil. It is known for research contribution in the topics: Population & Dry matter. The organization has 16012 authors who have published 26711 publications receiving 353416 citations.

Efeito da alteração ambiental sobre comunidades de Odonata em riachos de Mata Atlântica de Minas Gerais, Brasil

Abstract: The effect of riparian deforestation and stream impoundments on an odonate community was studied in areas of surviving Atlantic forest in Vicosa and in Rio Doce State Park (PERD), Marlieria, Minas Gerais, Brazil. During 1997 16 species of Libellulidae, 4 Coenagrionidae, 2 Gomphidae, 2 Calopterygidae, 1 Megapodagrionidae, 1 Aeshnidae and 3 Protoneuridae were collected. In Vicosa, the association of sampled odonates with lotic or lentic systems, and in PERD for areas with or without riparian vegetation were compared. The results suggest that although overall odonate taxonomic richness is high in areas without riparian vegetation. Likely, because productivity increase of such areas and its invasion by lentic Odonata species.

The Binding Protein BiP Attenuates Stress-Induced Cell Death in Soybean via Modulation of the N-Rich Protein-Mediated Signaling Pathway

Abstract: The molecular chaperone binding protein (BiP) participates in the constitutive function of the endoplasmic reticulum (ER) and protects the cell against stresses. In this study, we investigated the underlying mechanism by which BiP protects plant cells from stress-induced cell death. We found that enhanced expression of BiP in soybean (Glycine max) attenuated ER stress- and osmotic stress-mediated cell death. Ectopic expression of BiP in transgenic lines attenuated the leaf necrotic lesions that are caused by the ER stress inducer tunicamycin and also maintained shoot turgidity upon polyethylene glycol-induced dehydration. BiP-mediated attenuation of stress-induced cell death was confirmed by the decreased percentage of dead cell, the reduced induction of the senescence-associated marker gene GmCystP, and reduced DNA fragmentation in BiP-overexpressing lines. These phenotypes were accompanied by a delay in the induction of the cell death marker genes N-RICH PROTEIN-A (NRP-A), NRP-B, and GmNAC6, which are involved in transducing a cell death signal generated by ER stress and osmotic stress through the NRP-mediated signaling pathway. The prosurvival effect of BiP was associated with modulation of the ER stress- and osmotic stress-induced NRP-mediated cell death signaling, as determined in transgenic tobacco (Nicotiana tabacum) lines with enhanced (sense) and suppressed (antisense) BiP levels. Enhanced expression of BiP prevented NRP- and NAC6-mediated chlorosis and the appearance of senescence-associated markers, whereas silencing of endogenous BiP accelerated the onset of leaf senescence mediated by NRPs and GmNAC6. Collectively, these results implicate BiP as a negative regulator of the stress-induced NRP-mediated cell death response.