Cell News | Issue 01, 2017 - page 27

Cell News 01/2017
Hormonal control of body size by the single extracellular
protein Obstructor-A in Drosophila
Yanina-Yasmin Pesch and Matthias Behr
Presenting author: Matthias Behr
Structural and Computational Biology, EMBL, Heidelberg
Identification of signals for systemic adaption of hormonal
regulation would help to understand the crosstalk between
organs and environmental conditions contributing growth,
metabolic homeostasis and developmental progress. In a
recent study we found that the apical extracellular matrix
Obstructor-A (Obst-A) controls animals growth by determining
cell number of the endocrine ring gland organ in Drosophila
melanogaster. We show that Obst-A is required to guide axonal
growth between neuroendocrine parts of the ring gland organ
that senses systemic glucose regulation, time control and hor-
mone production. Obst-A function in the ring gland ultimately
directs ecdysone response for larval growth control and sur-
vival. Upregulation of genes controlling ecdysone biosynthesis
and signaling were disturbed in the absence of obst-A. Con-
sequently, gene encoding hormones triggering cuticle molting
at the periphery were not activated. Our studies demonstrate
that Obst-A provokes hormonal response at initial steps of
larval development, although it is itself possibly target of the
ecdysone machinery at the cuticle. These findings suggest that
Obst-A plays a central role in a yet unknown control mecha-
nism between ring gland and periphery that precisely decides
developmental progress.
Bidirectional Communications Of Macrophages And
Mesenchymal Stromal Cells In Direct And Indirect
Co-Culture System
Tina Tylek*, Katrin Schlegelmilch*, Andrea Ewald*, Franz Jakob+, Jürgen Groll*
*: Universitätsklinikum Würzburg, Zahnklinik, Abteilung für Funktionswerkstoffe der Medizin und Zahnheilkunde,
Pleicherwall 2, 97070 Würzburg
+: Orthopädische Klinik König-Ludwig-Haus Würzburg, Brettreichstraße 11, 97074 Würzburg
Presenting author: Tina Tylek
Universitätsklinikum Würzburg, Zahnklinik, Abteilung für
Funktionswerkstoffe der Medizin und Zahnheilkunde,
97070 Würzburg
Monocytes and the arising macrophages are important cells of
the innate immune system. The latter participate in the elimi-
nation of pathogens by phagocytosis, initiation of inflammato-
ry reactions, as well as tissue repair and can be classified into
inflammatory M1 and anti-inflammatory M2 macrophages.
Together with multipotent human mesenchymal stromal cells
(MSC), macrophages trigger tissue renewal and anti-inflamma-
tory reactions.
In our approach, we used three different co-culture models
for investigation of the reactions between macrophages and
MSCs: direct co-culture, the transwell-system and the use
of conditioned media. Via these models, we examined the
mitochondria transfer from one cell type to each other and the
influence of hMSC presence on the phagocytic activity. By flow
cytometry and fluorescence microscopy it could be shown, that
both hMSCs and most notably also macrophages release mito-
chondria and internalize them in direct, via tunneling nano-
tubes, as well as in indirect contact. After only three hours of
co-culture, the majority of the cells showed a mitochondrial
uptake. Examined due to the isolation of extracellular vesi-
cles, we could show that Mitochondria were released into the
medium and could be transferred via conditioned medium.
Co-cultivation by means of the different systems leads to an
increase of phagocytic activity of macrophages. For investiga-
tion of phagocytosis we used 2 µm red-fluorescent latex beads.
Macrophages showed the highest phagocytic rate and the
strongest increase after direct co-cultivation.
Within this project, it could be shown that both cell types
interact with each other by direct and indirect ways. The
used methods: examination of mitochondrial transfer and the
phagocytose assay are suitable for analyzation of the inter-
actions between hMSCs and macrophages in 2D as well as in
We thank the European Research Council (ERC, consolidator
grant Design2Heal, contract no 617989) for funding of this
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