Tissue-specific transcription of the neuronal gene Lim3 affects Drosophila melanogaster lifespan and locomotion
| Autor: | Alexander V. Symonenko, Elena G. Pasyukova, Olga Y. Rybina, A. V. Krementsova, S. V. Sarantseva, Olga I. Bolschakova, Elena V Ryabova, Ekaterina R. Veselkina, Natalia V. Roshina |
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| Rok vydání: | 2017 |
| Předmět: |
Male
0301 basic medicine Nervous system Aging Candidate gene Cell type Transcription Genetic LIM-Homeodomain Proteins Longevity Neuromuscular Junction Real-Time Polymerase Chain Reaction Animals Genetically Modified 03 medical and health sciences RNA interference medicine Animals Drosophila Proteins Transcription factor Neurons Genetics Gene knockdown biology Reverse Transcriptase Polymerase Chain Reaction Motor neuron biology.organism_classification Cell biology Drosophila melanogaster 030104 developmental biology medicine.anatomical_structure Larva Female Geriatrics and Gerontology Gerontology Locomotion Transcription Factors |
| Zdroj: | Biogerontology. 18:739-757 |
| ISSN: | 1573-6768 1389-5729 |
| DOI: | 10.1007/s10522-017-9704-x |
| Popis: | The identity of neuronal cell types is established and maintained by the expression of neuronal genes coding for ion channels, neurotransmitters, and neuropeptides, among others. Some of these genes have been shown to affect lifespan; however, their role in lifespan control remains largely unclear. The Drosophila melanogaster gene Lim3 encodes a transcription factor involved in complicated motor neuron specification networks. We previously identified Lim3 as a candidate gene affecting lifespan. To obtain direct evidence of the involvement of Lim3 in lifespan control, Lim3 overexpression and RNAi knockdown were induced in the nervous system and muscles of Drosophila using the GAL4-UAS binary system. We demonstrated that Lim3 knockdown in the nervous system increased survival at an early age and that Lim3 knockdown in muscles both increased survival at an early age and extended median lifespan, directly establishing the involvement of Lim3 in lifespan control. Lim3 overexpression in nerves and muscles was deleterious and led to lethality and decreased lifespan, respectively. Lim3 misexpression in both nerves and muscles increased locomotion regardless of changes in lifespan, which indicated that the effects of Lim3 on lifespan and locomotion can be uncoupled. Decreased synaptic activity was observed in the neuromuscular junctions of individuals with Lim3 overexpression in muscles, in association with decreased lifespan. However, no changes in NMJ activity were associated with the positive shift in locomotion observed in all misexpression genotypes. Our data suggested that modifications in the microtubule network may be induced by Lim3 misexpression in muscles and cause an increase in locomotion. |
| Databáze: | OpenAIRE |
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