We have isolated cDNAs encoding a second member of the dilute (myosin-V) unconventional myosin family in vertebrates, myr 6 (Myosin from rat 6). Expression of myr 6 transcripts in the brain is much more limited than is the expression of dilute, with highest levels observed in choroid plexus and components of the limbic system. We have mapped the myr 6 locus to mouse chromosome 18 using an interspecific backcross. The 3' portion of the myr 6 cDNA sequence from rat is nearly identical to that of a previously published putative glutamic acid decarboxylase from mouse
Bright/ARID3A is a nuclear matrix-associated transcription factor that stimulates immunoglobulin heavy chain (IgH) expression and Cyclin E1/E2F-dependent cell cycle progression. Bright positively activates IgH transcriptional initiation by binding to ATC-rich P sites within nuclear matrix attachment regions (MARs) flanking the IgH intronic enhancer (Eμ). Over-expression of Bright in cultured B cells was shown to correlate with DNase hypersensitivity of Eμ. We report here further efforts to analyze Bright-mediated Eμ enhancer activation within the physiological constraints of chromatin. A system was established in which VH promoter-driven in vitro transcription on chromatin-reconstituted templates was responsive to Eμ. Bright assisted in blocking the general repression caused by nucleosome assembly but was incapable of stimulating transcription from prebound nucleosome arrays. In vitro transcriptional derepression by Bright was enhanced on templates in which Eμ is flanked by MARs and was inhibited by competition with high affinity Bright binding (P2) sites. DNase hypersensitivity of chromatin-reconstituted Eμ was increased when prepackaged with B cell nuclear extract supplemented with Bright. These results identify Bright as a contributor to accessibility of the IgH enhancer.
The epoch of adolescent brain development is an ideal time to train complex thinking skills, and middle schools provide an ideal environment to train and foster this acquisition. Unfortunately, few teachers are equipped with enough knowledge of the science of learning and evidence-based methodology, to ensure all students are given sufficient opportunity to develop their cognitive capacity to the fullest. Using our evidenced-based higher-order executive function training program, we trained current teachers to provide cognitive training to their students. The results of this study demonstrate the efficacy of teacher-implemented intervention for immediate improvement in high-level executive function capacities such as gist-reasoning and interpretive statement production. More importantly, we found evidence of far transfer via students’ improved academic performance in all standardized test content areas (Reading, Mathematics, Science, and Social Studies) when compared to their untrained peers. Our findings support the importance of providing intensive professional development that afford educators with a greater understanding of the brain, how we learn, and the importance of evidence-based programs to advance and instill high-level executive function in all students.
We have isolated two cDNAs that encode putative myosin I heavy chains by polymerase chain reaction amplification of brain cDNA with degenerate oligodeoxynucleotide primers representing myosin I‐speeific conserved amino acid sequences. We report the complete deduced amino acid sequence of one of these cDNAs. The sequence is most similar to those of the avian and bovine brush border myosin Is, with five putative calmodulin‐binding repeats at the head‐tail junction. Northern analysis demonstrates that this myosin heavy chain, unlike the brush border myosins, is expressed in many tissues.
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