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Guerra, F.

Publications and source records attributed to Guerra, F..

2 recordsLinked to original sources

A Library of Electrophysiological Responses in Plants - A Model of Transversal Education and Open Science

Electrophysiology in plants is understudied, and, moreover, an ideal model for student inclusion at all levels of education. Here we report on an investigation in "open science", whereby scientists worked with students and faculty from Chile, Germany, Serbia, South Korea, and the USA. The students recorded the electrophysiological signals of >15 plants in response to a flame or tactile stimulus applied to the leaves. We observed that approximately 60% of the plants studied showed an electrophysiological response with a delay of [~]3-6 seconds after stimulus presentation. In preliminary conduction velocity experiments, we verified that observed signals are indeed biological in origin, with information transmission speeds of [~]2-9 mm/s. Such easily replicable experiments can serve to include more investigators and students in contributing to our understanding of plant electrophysiology.

plant biology↗

Mitochondria dysfunction in Charcot Marie Tooth 2B Peripheral Sensory Neuropathy

Recent evidence has uncovered an important role of Rab7 in regulating mitochondrial morphology and function. Missense mutation(s) of Rab7 underlies the pathogenesis of Charcot Marie Tooth 2B (CMT2B) peripheral neuropathy. Herein, we investigated how mitochondrial morphology and function were impacted by the CMT2B associated Rab7V162M mutation in fibroblasts from human CMT2B patients as well as in a knockin mouse model. In contrast to recently published results from studies of using heterologous overexpression systems, our results have demonstrated significant mitochondrial fragmentation in fibroblasts of both human CMT2B patients and CMT2B mouse embryonic fibroblasts (MEFs). Furthermore, we have shown that mitochondria were fragmented and axonal mitochondrial movement was dysregulated in primary cultured E18 dorsal root ganglion (DRG) sensory neurons, but not in E18 hippocampal and cortical primary neurons. We also show that inhibitors to either the mitochondrial fission protein Drp1 or to the nucleotide binding to Rab7 normalized the mitochondrial deficits in both MEFs and E18 cultured DRG neurons. Our study has revealed, for the first time, that expression of CMT2B Rab7 mutation at physiological level enhances Drp1 activity to promote mitochondrial fission, that may potentially underlie selective vulnerability of peripheral sensory neurons in CMT2B pathogenesis.

neuroscience↗