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At least 163 records · Page 9Linked to original sources
PubMed2003

RhoD regulates endosome dynamics through Diaphanous-related Formin and Src tyrosine kinase.

Early endosomes move bidirectionally between the cell periphery and the interior through a mechanism regulated by the low molecular weight GTPase RhoD. Here, we identify a novel splice variant of human Diaphanous, hDia2C, which specifically binds to RhoD and is recruited onto early endosomes. Expression of RhoD and hDia2C induces a striking alignment of early endosomes along actin filaments and reduces their motility. This activity depends on the membrane recruitment and activation of c-Src kinase, thus uncovering a new role in endosome function. Our results define a novel signal transduction pathway, in which hDia2C and c-Src are sequentially activated by RhoD to regulate the motility of early endosomes through interactions with the actin cytoskeleton.

Amino Acid Sequence↗
PubMed1968

Production of nuclease-formine 5'-nucleotide by Aspergillus quercinus in a low phosphate medium.

The production of ribonucleic acid (RNA)-depolymerase-forming 5'-nucleotides (5'-nuclease) was investigated with the fungus Aspergillus quercinus in media containing 68, 10, 5, 3, 1, and 0.5 mg of phosphorus per 100 ml. Yields were maximal with 5 mg of phosphorus per 100 ml. RNA-depolymerase-forming 3'-nucleosides (3'-nuclease) and phosphomonoesterase were maximal in media containing 1 and 0.5 mg of phosphorus per 100 ml. The 5'-nuclease was purified approximately 530-fold with a recovery of 84% by column chromatography on diethylaminoethyl-cellulose and by gel filtration through Sephadex G-100. The purified enzyme was capable of acting on both deoxyribonucleic acid and RNA, and the 5'-mononucleotides produced were identified by paper chromatography. The enzyme 5'-nuclease appears to be one of the repressible exonucleases that are active in the production of 5'-mononucleotides.

Aspergillus↗
PubMed2004

Mouse limb deformity mutations disrupt a global control region within the large regulatory landscape required for Gremlin expression.

The mouse limb deformity (ld) mutations cause limb malformations by disrupting epithelial-mesenchymal signaling between the polarizing region and the apical ectodermal ridge. Formin was proposed as the relevant gene because three of the five ld alleles disrupt its C-terminal domain. In contrast, our studies establish that the two other ld alleles directly disrupt the neighboring Gremlin gene, corroborating the requirement of this BMP antagonist for limb morphogenesis. Further doubts concerning an involvement of Formin in the ld limb phenotype are cast, as a targeted mutation removing the C-terminal Formin domain by frame shift does not affect embryogenesis. In contrast, the deletion of the corresponding genomic region reproduces the ld limb phenotype and is allelic to mutations in Gremlin. We resolve these conflicting results by identifying a cis-regulatory region within the deletion that is required for Gremlin activation in the limb bud mesenchyme. This distant cis-regulatory region within Formin is also altered by three of the ld mutations. Therefore, the ld limb bud patterning defects are not caused by disruption of Formin, but by alteration of a global control region (GCR) required for Gremlin transcription. Our studies reveal the large genomic landscape harboring this GCR, which is required for tissue-specific coexpression of two structurally and functionally unrelated genes.

Amino Acid Sequence↗