RESUMO
Alternative splicing is an important regulatory process that produces multiple transcripts from a single gene, significantly modulating the transcriptome and potentially the proteome, during development and in response to environmental cues. In the first part of this review, we summarize recent advances and highlight the accumulated knowledge on the biological roles of alternative splicing isoforms that are key for different plant responses and during development. Remarkably, we found that many of the studies in this area use similar methodological approaches that need to be improved to gain more accurate conclusions, since they generally presume that stable isoforms undoubtedly have coding capacities. This is mostly done without data indicating that a particular RNA isoform is in fact translated. So, in the latter part of the review, we propose a thorough strategy to analyze, evaluate, and characterize putative functions for alternative splicing isoforms of interest.
Assuntos
Processamento Alternativo , Arabidopsis , Arabidopsis/genética , Isoformas de Proteínas/genética , Isoformas de Proteínas/metabolismo , Plantas/genética , Plantas/metabolismoRESUMO
Nicotine exposure is associated with numerous neurodevelopmental aberrations, including impairment of the neuroventilatory response to hypercapnia in bullfrog tadpoles and mouse neonates following prolonged developmental exposure. It is unclear how acute nicotine exposure affects neuroventilation and the neuroventilatory response to hypercapnia, or how these effects might differ from those of chronic exposure. In this study the neural correlates of ventilation were recorded from in vitro brainstem preparations derived from early and late metamorphic tadpoles and juvenile bullfrogs. Lung and gill/buccal breath parameters were compared during control (=0), 18, 50, 100, and 200microg/L nicotine conditions, applied during normocapnia (1.5% CO(2)) and hypercapnia (5.0% CO(2)). All preparations demonstrated a reduction in normocapnic lung burst frequency and an attenuated hypercapnic response during acute nicotine treatment. The concentrations necessary to elicit both of these responses decreased from 200microg/L nicotine in early metamorphic tadpole brainstems to 18microg/L nicotine in juvenile bullfrog brainstems, which suggests a developmental increase in acute nicotine sensitivity that is distinguishable from the developmental changes in vulnerability to chronic nicotine exposure. In summary, acute nicotine exposure impaired central CO(2) response, attenuated rather than enhanced respiratory drive, and had more pronounced effects at progressively lower concentrations as development proceeded through metamorphosis.