Title |
Compensatory growth in novel Drosophila Akt1 mutants
|
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Published in |
BMC Research Notes, March 2015
|
DOI | 10.1186/s13104-015-1032-0 |
Pubmed ID | |
Authors |
Jennifer D Slade, Brian E Staveley |
Abstract |
Organisms, tissues and cells are genetically programmed to grow to a specific largely pre-set size and shape within the appropriate developmental timing. In the event of mutation, cell death, or tissue damage, the remaining cells may increase their rate of growth to compensate and generate an intact, potentially smaller, tissue or organism in order to achieve the desired size. A delay in the developmental timing could aid in this process. The insulin receptor signalling pathway with its central component, the Akt1 kinase, and endpoint regulator, the transcription factor foxo, plays a significant role in the control of growth. Drosophila melanogaster is an excellent model organism with a well-studied life cycle and a consistently developing compound eye that can undergo analysis to compare changes in the properties of adult ommatidia as an indicator of growth. |
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