Real-Time, Real World Learning—Capitalising on Mobile Technology

This chapter explores the adoption of Web 2.0 technologies to promote active learning by students and to both mediate and enhance classroom instruction. Web 2.0 refers to open source, web-enabled applications (apps) that are driven by user-manipulated and user-generated content (Kassens-Noor, 2012). These apps are often rich in user participation, have dynamic content, and harness the collective intelligence of users (Chen, Hwang, & Wang, 2012). As such, these processes create “active, context based, personalised learning experiences” (Kaldoudi, Konstantinidis, & Bamidis, 2010, p. 130) that prioritise learning ahead of teaching. By putting the learner at the centre of the education process educators can provide environments that enhance employability prospects and spark a passion for learning that, hopefully, lasts a lifetime. As such, we critique an active learning approach that makes use of technology such as mobile applications (apps), Twitter, and augmented reality to enhance students’ real world learning. Dunlap and Lowenthal (2009) argue that social media can facilitate active learning as they recreate informal, free-flowing communications that allow students and academics to connect on a more emotional level. Furthermore, their use upskills students in the technical complexities of the digital world and also the specialised discourses that are associated with online participation, suitable for real world learning and working (Fig. 16.1). Three case studies explore the benefits of Web 2.0 processes. The first details the use of Twitter chats to connect students, academics, and industry professionals via online synchronous discussions that offer a number of benefits such as encouraging concise writing from students and maintaining on-going relationships between staff, students, and industry contacts. The second details a location-based mobile app that delivers content to students when they enter a defined geographical boundary linked to an area of a sports precinct. Finally, we explore the use of augmented reality apps to enhance teaching in Human Geography and Urban Studies

Misguided Transcriptional Elongation Causes Mixed Lineage Leukemia

Investigation of the activity of a family of fusion proteins that cause aggressive leukemia suggests transcriptional elongation as a new mechanism for oncogenic transformation

New Insights into the Control of HIV-1 Transcription: When Tat Meets the 7SK snRNP and Super Elongation Complex (SEC)

Recent studies aimed at elucidating the mechanism controlling HIV-1 transcription have led to the identification and characterization of two multi-subunit complexes that both contain P-TEFb, a human transcription elongation factor and co-factor for activation of HIV-1 gene expression by the viral Tat protein. The first complex, termed the 7SK snRNP, acts as a reservoir where active P-TEFb can be withdrawn by Tat to stimulate HIV-1 transcription. The second complex, termed the super elongation complex (SEC), represents the form of P-TEFb delivered by Tat to the paused RNA polymerase II at the viral long terminal repeat during Tat transactivation. Besides P-TEFb, SEC also contains other elongation factors/co-activators, and they cooperatively stimulate HIV-1 transcription. Recent data also indicate SEC as a target for the mixed lineage leukemia (MLL) protein to promote the expression of MLL target genes and leukemogenesis. Given their roles in HIV-1/AIDS and cancer, further characterization of 7SK snRNP and SEC will help develop strategies to suppress aberrant transcriptional elongation caused by uncontrolled P-TEFb activation. As both complexes are also important for normal cellular gene expression, studying their structures and functions will elucidate the mechanisms that control metazoan transcriptional elongation in general

MCEF is localized to the nucleus by protein sequences encoded within three distinct exons, where it represses HIV-1 Tat-transactivation of LTR-directed transcription

<p>Translocations between the human Mixed Lineage Leukemia (MLL) and AF4 Family (AFF) member genes, are implicated in leukemia. Mutations to AFFs can disrupt lymphopoesis, CNS development and spermatogenesis. However, despite the growing list of pathologies linked to AFF members, their evolutionary relationship and the structure/function of individual members, remain to be elucidated. Here, we first report that database mining and phylogenetic analysis with AFF proteins from multiple species, revealed two monophyletic sister clades, suggesting a common<i> Bilateria </i>ancestor. We then examined the structure/function of the most recently discovered AFF member, MCEF (also known as AF5q31 or AFF4). <i>In silico</i>, the human MCEF gene was found to have 21 exons, and code for a protein with seven nuclear localization sequences (NLS). In HeLa cells, an MCEF-EGFP fusion protein, localized exclusively to the nucleus. Consequently, we made twenty constructs, expressing MCEF deletion mutants fused to EGFP and/or DsRed fluorescent proteins. Three distinct protein sequences, encoded by three separate MCEF exons, were found to mediate nuclear localization, only two of which were predicted <i>in silico</i>. Importantly, we also found that ectopic expression of MCEF, repressed HIV-1 LTR-directed RNA Polymerase II transcription, at the level of Tat-transactivation. We suggest that portions of MCEF could be exploited for chimeric transcription factor repression (CTFR) of HIV-1.</p