title: Cell death regulates muscle fiber number.
abstract: Cell death can have both cell autonomous and non-autonomous roles in normal development. Previous studies have shown that the central cell death regulators grim and reaper are required for the developmentally important elimination of stem cells and neurons in the developing central nervous system (CNS). Here we show that cell death in the nervous system is also required for normal muscle development. In the absence of grim and reaper, there is an increase in the number of fibers in the ventral abdominal muscles in the Drosophila adult. This phenotype can be partially recapitulated by inhibition of cell death specifically in the CNS, indicating a non-autonomous role for neuronal death in limiting muscle fiber number. We also show that FGFs produced in the cell death defective nervous system are required for the increase in muscle fiber number. Cell death in the muscle lineage during pupal stages also plays a role in specifying fiber number. Our work suggests that FGFs from the CNS act as a survival signal for muscle founder cells. Thus, proper muscle fiber specification requires cell death in both the nervous system and in the developing muscle itself.
authors.affiliation: CBRC, Massachusetts General Hospital Research Institute/Harvard Medical School, Boston, MA 02129, USA.
authors.forename: Tatevik
authors.initials: T
authors.lastname: Sarkissian
authors.affiliation: CBRC, Massachusetts General Hospital Research Institute/Harvard Medical School, Boston, MA 02129, USA.
authors.forename: Richa
authors.initials: R
authors.lastname: Arya
authors.affiliation: CBRC, Massachusetts General Hospital Research Institute/Harvard Medical School, Boston, MA 02129, USA.
authors.forename: Seda
authors.initials: S
authors.lastname: Gyonjyan
authors.affiliation: Department of Integrative Biology, Oregon State University, Corvallis, OR 97331, USA.
authors.forename: Barbara
authors.initials: B
authors.lastname: Taylor
authors.affiliation: CBRC, Massachusetts General Hospital Research Institute/Harvard Medical School, Boston, MA 02129, USA. Electronic address: kristin.white@mgh.harvard.edu.
authors.forename: Kristin
authors.initials: K
authors.lastname: White
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002452:Cell Count; D029721:Drosophila Proteins / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D004331:Drosophila melanogaster / Q000166:cytology / Q000196:embryology / Q000235:genetics / Q000254:growth & development*; D005346:Fibroblast Growth Factors / Q000502:physiology; D018507:Gene Expression Regulation, Developmental; D005971:Glutamates / Q000502:physiology; D007814:Larva; D008164:Luminescent Proteins / Q000032:analysis; D009046:Motor Neurons / Q000166:cytology; D032342:Muscle Cells / Q000648:ultrastructure*; D024510:Muscle Development; D009132:Muscles / Q000294:innervation; D032446:Myoblasts / Q000166:cytology; D009479:Neuropeptides / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D011505:Protein-Tyrosine Kinases / Q000172:deficiency / Q000502:physiology; D011679:Pupa; D017468:Receptors, Fibroblast Growth Factor / Q000172:deficiency / Q000502:physiology; D017384:Sequence Deletion
chemical_list: D029721:Drosophila Proteins; D005971:Glutamates; D008164:Luminescent Proteins; D009479:Neuropeptides; D017468:Receptors, Fibroblast Growth Factor; C108881:grim protein, Drosophila; C086973:rpr protein, Drosophila; D005346:Fibroblast Growth Factors; D011505:Protein-Tyrosine Kinases; C102667:htl protein, Drosophila
keywords: Apoptosis; Drosophila; FGF; Muscle