Alternative trans-splicing of Caenorhabditis elegans sma-9/schnurri generates a short transcript that provides tissue-specific function in BMP signaling

<p>Abstract</p> <p>Background</p> <p>Transcription cofactors related to <it>Drosophila </it>Schnurri facilitate the transcriptional programs regulated by BMP signaling in <it>C. elegans</it>, <it>Drosophila</it>, Xenopus, and mouse. In different systems, Schnurri homologs have been shown to act as either agonists or antagonists of Smad function, and as either positive or negative regulators of transcription. How Schnurri proteins achieve this diversity of activities is not clear. The <it>C. elegans sma-9/schnurri </it>locus undergoes alternative splicing, including an unusual <it>trans</it>-splicing event that could generate two non-overlapping shorter transcripts.</p> <p>Results</p> <p>We demonstrate here that the shorter transcripts are expressed <it>in vivo</it>. Furthermore, we find that one of the short transcripts plays a tissue-specific role in <it>sma-9 </it>function, contributing to the patterning of male-specific sensory rays, but not to the regulation of body size. Based on previous results, we suggest that this transcript encodes a C-terminal SMA-9 isoform that may provide transcriptional activation activity, while full length isoforms may mediate transcriptional repression and/or activation in a context-dependent manner.</p> <p>Conclusion</p> <p>The alternative <it>trans</it>-splicing of <it>sma-9 </it>may contribute to the diversity of functions necessary to mediate tissue-specific outputs of BMP signaling.</p

TGF-β pathways in aging and immunity: lessons from Caenorhabditis elegans

The Transforming Growth Factor-β (TGF-β) superfamily of signaling molecules plays critical roles in development, differentiation, homeostasis, and disease. Due to the conservation of these ligands and their signaling pathways, genetic studies in invertebrate systems including the nematode Caenorhabditis elegans have been instrumental in identifying signaling mechanisms. C. elegans is also a premier organism for research in longevity and healthy aging. Here we summarize current knowledge on the roles of TGF-β signaling in aging and immunity

Chloride intracellular channel proteins respond to heat stress in Caenorhabditis elegans

Chloride intracellular channel proteins (CLICs) are multi-functional proteins that are expressed in various cell types and differ in their subcellular location. Two CLIC homologs, EXL-1 (excretory canal abnormal like-1) and EXC-4 (excretory canal abnormal± 4), are encoded in the Caenorhabditis elegans genome, providing an excellent model to study the functional diversification of CLIC proteins. EXC-4 functions in excretory canal formation during normal animal development. However, to date, the physiological function of EXL-1 remains largely unknown. In this study, we demonstrate that EXL-1 responds specifically to heat stress and translocates from the cytoplasm to the nucleus in intestinal cells and body wall muscle cells under heat shock. In contrast, we do not observe EXC-4 nuclear translocation under heat shock. Full protein sequence analysis shows that EXL-1 bears a non-classic nuclear localization signal (NLS) that EXC-4 is lacking. All mammalian CLIC members have a nuclear localization signal, with the exception of CLIC3. Our phylogenetic analysis of the CLIC gene families across various animal species demonstrates that the duplication of CLICs in protostomes and deuterostomes occurred independently and that the NLS was subsequently lost in amniotes and nematodes, suggesting convergent evolution. We also observe that EXL-1 nuclear translocation occurs in a timely ordered manner in the intestine, from posterior to anterior regions. Finally, we find that exl-1 loss of function mutants are more susceptible to heat stress than wild-type animals, demonstrating functional relevance of the nuclear translocation. This research provides the first link between CLICs and environmental heat stress. We propose that C. elegans CLICs evolved to achieve different physiological functions through subcellular localization change and spatial separation in response to external or internal signals

A role for sperm in regulation of egg-laying in the Nematode C. elegans

Background In insects and in mammals, male sperm and seminal fluid provide signaling factors that influence various aspects of female physiology and behavior to promote reproductive success and to compete with other males. It is less apparent how important such signaling is in the context of a self-fertile hermaphrodite species. We have addressed this question in the nematode Caenorhabditis elegans, which can reproduce either by hermaphrodite self-fertilization or by male-hermaphrodite mating. Results We have studied the egg-laying defective mutant, egl-32, and found that the cellular basis of the egl-32 egg-laying phenotype is likely a defect in sperm. First, the time of egl-32 action coincides with the timing of spermatogenesis in the hermaphrodite. Second, egl-32 interacts with genes expressed in sperm. Third, mating experiments have revealed that wild-type sperm can rescue the egg-laying defect of egl-32 mutant animals. Most importantly, introduction of mutant egl-32 sperm into wild-type hermaphrodites or females is sufficient to induce an egg-laying defective phenotype. Conclusion Previous work has revealed that C. elegans sperm release factors that stimulate oocyte maturation and ovulation. Here we describe evidence that sperm also promote egg laying, the release of embryos from the uterus

Meisosomes, folded membrane microdomains between the apical extracellular matrix and epidermis

Apical extracellular matrices (aECMs) form a physical barrier to the environment. In Caenorhabditis elegans, the epidermal aECM, the cuticle, is composed mainly of different types of collagen, associated in circumferential ridges separated by furrows. Here, we show that in mutants lacking furrows, the normal intimate connection between the epidermis and the cuticle is lost, specifically at the lateral epidermis, where, in contrast to the dorsal and ventral epidermis, there are no hemidesmosomes. At the ultrastructural level, there is a profound alteration of structures that we term 'meisosomes,' in reference to eisosomes in yeast. We show that meisosomes are composed of stacked parallel folds of the epidermal plasma membrane, alternately filled with cuticle. We propose that just as hemidesmosomes connect the dorsal and ventral epidermis, above the muscles, to the cuticle, meisosomes connect the lateral epidermis to it. Moreover, furrow mutants present marked modifications of the biomechanical properties of their skin and exhibit a constitutive damage response in the epidermis. As meisosomes co-localise to macrodomains enriched in phosphatidylinositol (4,5) bisphosphate, they could conceivably act, like eisosomes, as signalling platforms, to relay tensile information from the aECM to the underlying epidermis, as part of an integrated stress response to damage

A role for sperm in regulation of egg-laying in the Nematode <it>C. elegans</it>

<p>Abstract</p> <p>Background</p> <p>In insects and in mammals, male sperm and seminal fluid provide signaling factors that influence various aspects of female physiology and behavior to promote reproductive success and to compete with other males. It is less apparent how important such signaling is in the context of a self-fertile hermaphrodite species. We have addressed this question in the nematode <it>Caenorhabditis elegans</it>, which can reproduce either by hermaphrodite self-fertilization or by male-hermaphrodite mating.</p> <p>Results</p> <p>We have studied the egg-laying defective mutant, <it>egl-32</it>, and found that the cellular basis of the <it>egl-32 </it>egg-laying phenotype is likely a defect in sperm. First, the time of <it>egl-32 </it>action coincides with the timing of spermatogenesis in the hermaphrodite. Second, <it>egl-32 </it>interacts with genes expressed in sperm. Third, mating experiments have revealed that wild-type sperm can rescue the egg-laying defect of <it>egl-32 </it>mutant animals. Most importantly, introduction of mutant <it>egl-32 </it>sperm into wild-type hermaphrodites or females is sufficient to induce an egg-laying defective phenotype.</p> <p>Conclusion</p> <p>Previous work has revealed that <it>C. elegans </it>sperm release factors that stimulate oocyte maturation and ovulation. Here we describe evidence that sperm also promote egg laying, the release of embryos from the uterus.</p