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Multiple effects of the transcription factor Dimmed and the insulin receptor on growth and differentiation vary among neuron types and developmental stages in Drosophila
Stockholms universitet, Naturvetenskapliga fakulteten, Zoologiska institutionen.ORCID-id: 0000-0002-3552-5347
Stockholms universitet, Naturvetenskapliga fakulteten, Zoologiska institutionen.
Stockholms universitet, Naturvetenskapliga fakulteten, Zoologiska institutionen.ORCID-id: 0000-0002-1147-7766
(Engelska)Manuskript (preprint) (Övrigt vetenskapligt)
Nationell ämneskategori
Biologiska vetenskaper
Forskningsämne
funktionell zoomorfologi
Identifikatorer
URN: urn:nbn:se:su:diva-125119OAI: oai:DiVA.org:su-125119DiVA, id: diva2:891863
Tillgänglig från: 2016-01-07 Skapad: 2016-01-07 Senast uppdaterad: 2019-12-10Bibliografiskt granskad
Ingår i avhandling
1. Morphological and functional effects of insulin signaling and the bHLH transcription factor Dimmed on different neuron types in Drosophila
Öppna denna publikation i ny flik eller fönster >>Morphological and functional effects of insulin signaling and the bHLH transcription factor Dimmed on different neuron types in Drosophila
2016 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

In Drosophila, the insulin signaling pathway is at the interface between dietary conditions and control of growth and development, reproduction, stress responses and life span. Eight insulin like peptides (Dilp1-8), an insulin tyrosine kinase receptor (dInR) and its downstream components, as well as a relaxin-like receptor type (Lgr3) form the core of this signaling. Here we showed that the dInR mediates post-mitotic cell growth specifically in about 300 peptidergic neurons expressing the basic helix loop helix (bHLH) transcription factor Dimmed (Paper I).  Overexpression of dInR in Dimm positive neurons leads to increased size of cell body, Golgi apparatus and nucleus, whereas dInR knockdown causes an opposite effect. Manipulation of downstream components of insulin signaling induces similar changes in Dimm positive neurons. This mechanism is nutrient dependent. In Paper II, we further investigate the relation between Dimmed and dInR for regulation of cell growth. Coexpressing Dimm and dInR in a range of Dimm negative neurons results in increased cell size in both larval and adult stages. We provide further evidence that dInR regulates cell growth in a Dimm dependent manner and that DILP6 from glia cells is involved in this regulation. In addition, we find that Dimm alone is capable of triggering cell growth in certain neuron types at different developmental stages. Furthermore, ectopic Dimm alone can block apoptosis.  Dimm is a known master regulator of peptidergic cell fate. In paper III we find that ectopic expression of Dimm in Dimm negative motor neurons results in transformation the neurons towards a neuroendocrine phenotype. They acquire enlarged axon terminations and boutons, lose both pre- and postsynaptic markers, and display diminished levels of wingless and its receptor dFrizzled. Furthermore they show increased expression of several Dimm targets. Finally, combined ectopic Dimm and dInR expression gives rise to stronger phenotypes. In paper IV we studied another DILP possibly involved in growth regulation, the under-investigated DILP1. We generated Dilp1-Gal4 lines and anti DILP1 antibodies and found that DILP1 is transiently expressed in brain insulin producing cells (IPCs) from pupal stages to newly hatched adult flies. Diapausing virgin female flies display a high expression level of dilp1/DILP1 over at least 9 weeks of adult life. DILP1 expression is also correlated with the persistence of larval/pupal fat body and its expression is regulated by other DILPs and short neuropeptide F (sNPF). Flies mutant in dilp1 display increased food intake, but decreased stress resistance and life span. We found no obvious role of DILP1 in growth regulation.

Ort, förlag, år, upplaga, sidor
Stockholm University, 2016. s. 41
Nyckelord
insulin signaling, Dimm, neuropeptide, insulin receptor, insulin-like peptide, drosophila
Nationell ämneskategori
Naturvetenskap Biologiska vetenskaper
Forskningsämne
funktionell zoomorfologi
Identifikatorer
urn:nbn:se:su:diva-125941 (URN)978-91-7649-283-3 (ISBN)
Disputation
2016-02-26, Ahlmannsalen, Geovetenskapens hus, Svante Arrhenius väg 12, Stockholm, 10:00 (Engelska)
Opponent
Handledare
Anmärkning

At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 2: Manuscript. Paper 3: Manuscript. Paper 4: Manuscript.

Tillgänglig från: 2016-02-03 Skapad: 2016-01-20 Senast uppdaterad: 2019-12-09Bibliografiskt granskad

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