2. Behavioral Biology TALKS - Deutsche Zoologische Gesellschaft

and turnip) by feeding on the plant’s roots. Due to this largely subterranean life of
the larvae and the long emergence period of the adult flies, control of D. radicum
with pesticides is quite ineffective.
We have chemically characterized numerous neuropeptides from the central nervous
system and neurohemal organs, as well as regulatory peptides from enteroendocrine
midgut cells of the D. radicum larva. By RP-HPLC and Maldi-TOF/TOF mass
spectrometry, combined with chemical peptide labeling using 4-sulfophenyl
isothiocyanate, 38 peptides could be identified, representing major insect peptide
families: allatostatin A, allatostatin C, FMRFamide-like peptides, kinin, CAPA peptides,
pyrokinins, sNPF, myosuppressin, corazonin, SIFamide, sulfakinins, tachykinins,
NPLP1-peptides, adipokinetic hormone and CCHamide1. We also found a new
peptide (Yamide) without characterised homologs in other insects.
The immunohistochemical analysis of the distribution of several classes of peptideimmunoreactive
neurons and enteroendocrine cells in the larva revealed a very
similar but not identical peptide distribution to Drosophila melanogaster.
Since peptides are regulators of many physiological and behavioural processes in
insects such as molting or feeding, our data may provide a basis for the development
of new specific peptide-based protection methods against the cabbage root fly and
its larva.
����179 Yvonne Knieper
mRNA-based 'gene transfer' as a new tool in CF therapy
Authors: Yvonne Knieper 1 , Nadine Bangel-Ruland 1 , Barbara Leciejewski 1 , Katja
Sobczak 1 , G. Leier 1 , J. Rosenecker 2 , Wolf-Michael Weber 1
Affiliation: 1 Institute of Animal Physiology, WWU Münster; 2 Ludwig-Maximilians
University, Department of Pediatrics, Munich
Cystic Fibrosis (CF) is caused by a mutation of the cystic fibrosis transmembrane
conductance regulator (CFTR), a Cl- channel in the apical membrane of airway
epithelial cells. The most common mutation ?F508 leads to an impaired processing,
following degradation of the protein, preventing the functional expression of the
CFTR channel.
In this study we transfected human CF airway epithelial cells (CFBE41o-) with wild
type (wt) CFTR-mRNA to investigate the insertion and functional expression of CFTR
into the apical membrane. Therefore, we carried out Ussing chamber measurements
to demonstrate the restoration of CFTR function and in parallel performed protein
biochemical experiments to verify the increase of CFTR protein amount in the apical
plasma membrane.
After transfection with wtCFTR-mRNA Ussing chamber experiments revealed an
increased CFTR current following cAMP activation (74%) when compared to
untransfected cells. This current appeared to be almost identical to the current of
control cells expressing wtCFTR (16HBE14o-). Furthermore, the CFTR activation was
sensitive to the specific Cl- channel blocker CFTRinh172, which decreased nearly
100% of the generated CFTR current and also reduced the electrophysiological
parameters capacitance and conductance, significantly.
In addition, the protein biochemical approaches showed a markedly increased CFTR
protein amount in the apical membrane. Using immunofluorescence techniques we
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