In metazoans, two apparently distinct mechanisms specify germ cell fate: Determinate specification (observed in animals including Drosophila, Caenorhabditis elegans, zebra fish, and Xenopus) uses cytoplasmic factors localized to specific regions of the egg, whereas epigenetic specification (observed in many basal metazoans, urodeles, and mammals) involves inductive interactions between cells. Much of our understanding of germ cell specification has emerged from studies of model organisms displaying determinate specification. In contrast, our understanding of epigenetic/inductive specification is less advanced and would benefit from studies of additional organisms. Freshwater planarians-widely known for their remarkable powers of regeneration-are well suited for studying the mechanisms by which germ cells can be induced. Classic experiments showed that planarians can regenerate germ cells from body fragments entirely lacking reproductive structures, suggesting that planarian germ cells could be specified by inductive signals. Furthermore, the availability of the genome sequence of the planarian Schmidtea mediterranea, coupled with the animal's susceptibility to systemic RNA interference (RNAi), facilitates functional genomic analyses of germ cell development and regeneration. Here, we describe recent progress in studies of planarian germ cells and frame some of the critical unresolved questions for future work.
Aberrant dopamine D receptor (DR) activity is associated with neuropsychiatric disorders, making those receptors targets for antipsychotic drugs. Here, we report that novel signaling through the intracellularly localized DR long isoform (DR) elicits extracellular signal-regulated kinase (ERK) activation and dendritic spine formation through Rabex-5/platelet-derived growth factor receptor-β (PDGFRβ)-mediated endocytosis in mouse striatum. We found that DR directly binds to and activates Rabex-5, promoting early-endosome formation. Endosomes containing DR and PDGFRβ are then transported to the Golgi apparatus, where those complexes trigger Gαi3-mediated ERK signaling. Loss of intracellular DR-mediated ERK activation decreased neuronal activity and dendritic spine density in striatopallidal medium spiny neurons (MSNs). In addition, dendritic spine density in striatopallidal MSNs significantly increased following treatment of striatal slices from wild-type mice with quinpirole, a DR agonist, but those changes were lacking in DR knockout mice. Moreover, intracellular DR signaling mediated effects of a typical antipsychotic drug, haloperidol, in inducing catalepsy behavior. Taken together, intracellular DR signaling through Rabex-5/PDGFRβ is critical for ERK activation, dendritic spine formation and neuronal activity in striatopallidal MSNs of mice.
The charge form factor of 4He has been extracted in the range 29 fm(-2) ≤ Q2 ≤ 77 fm(-2) from elastic electron scattering, detecting 4He recoil nuclei and electrons in coincidence with the high resolution spectrometers of the Hall A Facility of Jefferson Lab. The measurements have uncovered a second diffraction minimum for the form factor, which was predicted in the Q2 range of this experiment. The data are in qualitative agreement with theoretical calculations based on realistic interactions and accurate methods to solve the few-body problem.
Introductory paragraphMuch of biology is associated with convergent traits, and it is challenging to determine the extent to which underlying molecular mechanisms are shared across phylogeny. By analyzing plants representing eighteen independent origins of C4 photosynthesis, we quantified the extent to which this convergent trait utilises identical molecular mechanisms. We demonstrate that biochemical changes that characterise C4 species are recovered by this process, and expand the paradigm by four metabolic pathways not previously associated with C4 photosynthesis. Furthermore, we show that expression of many genes that distinguish C3 and C4 species respond to low CO2, providing molecular evidence that reduction in atmospheric CO2 was a driver for C4 evolution. Thus the origin and architecture of complex traits can be derived from transcriptome comparisons across natural diversity.
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