Composition of cuticular lipids in the pteromalid wasp Lariophagus distinguendus is host dependent.

The insect cuticle is covered by a thin layer of hydrocarbons not only preventing desiccation but also playing an important role in the sexual communication of several species. In the pteromalid wasp Lariophagus distinguendus, a parasitoid of grain infesting beetles, female cuticular hydrocarbons (CHCs) elicit male courtship behaviour. We analyzed the CHC profiles of male and female L. distinguendus wasps reared on different beetle hosts by coupled gas chromatography- mass spectrometry (GC-MS). Statistical analysis of the data revealed significant differences between strains reared on different hosts, while spatially isolated strains reared on the same host produced similar profiles. CHC profiles of parasitoids reared on Stegobium paniceum were statistically distinguishable from those of wasps reared on all other hosts. A host shift from Sitophilus granarius to S. paniceum resulted in distinguishable CHC profiles of L. distinguendus females after only one generation. Considering the role of CHCs as contact sex pheromones, our data suggest that host shifts in parasitic wasps might lead to reproductive isolation of host races due to the modification of the cuticular semiochemistry.

Temporally controlled somatic mutagenesis in smooth muscle.

Ligand-dependent site-specific recombinases are powerful tools to engineer the mouse genome in specific somatic cell types at selected times during pre- and postnatal development. Current efforts are primarily directed towards increasing the efficiency of this recombination system in mice. We have generated transgenic mouse lines expressing a tamoxifen-activated Cre recombinase, CreER(T2), under the control of the smooth muscle-specific SM22 promoter. Both a randomly integrated transgene [SM-CreER(T2)(tg)] and a transgene that has been "knocked in" into the endogenous SM22 locus [SM-CreER(T2)(ki)] were expressed in smooth muscle-containing tissues. The level of CreER(T2) expression and tamoxifen-induced recombination was lower in SM-CreER(T2)(tg) mice compared with SM-CreER(T2)(ki) mice. Whereas no recombinase activity could be detected in vehicle-treated SM-CreER(T2)(ki) mice, administration of tamoxifen induced the excision of a loxP-flanked reporter transgene in up to 100% of smooth muscle cells. The recombined genome persisted for at least four months after tamoxifen treatment. SM-CreER(T2)(ki) transgenic mice should be useful to study the effects of various somatic mutations in smooth muscle.

Functional embryonic cardiomyocytes after disruption of the L-type alpha1C (Cav1.2) calcium channel gene in the mouse.

The L-type alpha(1C) (Ca(v)1.2) calcium channel is the major calcium entry pathway in cardiac and smooth muscle. We inactivated the Ca(v)1.2 gene in two independent mouse lines that had indistinguishable phenotypes. Homozygous knockout embryos (Ca(v)1. 2-/-) died before day 14.5 postcoitum (p.c.). At day 12.5 p.c., the embryonic heart contracted with identical frequency in wild type (+/+), heterozygous (+/-), and homozygous (-/-) Ca(v)1.2 embryos. Beating of isolated embryonic cardiomyocytes depended on extracellular calcium and was blocked by 1 microm nisoldipine. In (+/+), (+/-), and (-/-) cardiomyocytes, an L-type Ba(2+) inward current (I(Ba)) was present that was stimulated by Bay K 8644 in all genotypes. At a holding potential of -80 mV, nisoldipine blocked I(Ba) of day 12.5 p.c. (+/+) and (+/-) cells with two IC(50) values of approximately 0.1 and approximately 1 microm. Inhibition of I(Ba) of (-/-) cardiomyocytes was monophasic with an IC(50) of approximately 1 microm. The low affinity I(Ba) was also present in cardiomyocytes of homozygous alpha(1D) (Ca(v)1.3) knockout embryos at day 12.5 p.c. These results indicate that, up to day 14 p.c., contraction of murine embryonic hearts requires an unidentified, low affinity L-type like calcium channel.