The many positive impacts of participating in outreach activities on postgraduate students

Postgraduate students are excellent role models for school students, where their passion and energy play a vital role in engaging younger students and spreading enthusiasm and excitement about science. However, participating in outreach is not a one way activity for these postgraduate students. Through focus groups we show that the postgraduate students perceive that there are many benefits for themselves. These benefits are identified and discussed. This paper also contrasts the postgraduate with their undergraduate counterpart in terms of their contributions to engagement activities

APC/CFZR-1 Controls SAS-5 Levels To Regulate Centrosome Duplication in Caenorhabditis elegans

As the primary microtubule-organizing center, centrosomes play a key role in establishing mitotic bipolar spindles that secure correct transmission of genomic content. For the fidelity of cell division, centrosome number must be strictly controlled by duplicating only once per cell cycle. Proper levels of centrosome proteins are shown to be critical for normal centrosome number and function. Overexpressing core centrosome factors leads to extra centrosomes, while depleting these factors results in centrosome duplication failure. In this regard, protein turnover by the ubiquitin-proteasome system provides a vital mechanism for the regulation of centrosome protein levels. Here, we report that FZR-1, the Caenorhabditis elegans homolog of Cdh1/Hct1/Fzr, a coactivator of the anaphase promoting complex/cyclosome (APC/C), an E3 ubiquitin ligase, functions as a negative regulator of centrosome duplication in the C. elegans embryo. During mitotic cell division in the early embryo, FZR-1 is associated with centrosomes and enriched at nuclei. Loss of fzr-1 function restores centrosome duplication and embryonic viability to the hypomorphic zyg-1(it25) mutant, in part, through elevated levels of SAS-5 at centrosomes. Our data suggest that the APC/CFZR-1 regulates SAS-5 levels by directly recognizing the conserved KEN-box motif, contributing to proper centrosome duplication. Together, our work shows that FZR-1 plays a conserved role in regulating centrosome duplication in C. elegans

Casein kinase II is required for proper cell division and acts as a negative regulator of centrosome duplication in Caenorhabditis elegans embryos

Centrosomes are the primary microtubule-organizing centers that orchestrate microtubule dynamics during the cell cycle. The correct number of centrosomes is pivotal for establishing bipolar mitotic spindles that ensure accurate segregation of chromosomes. Thus, centrioles must duplicate once per cell cycle, one daughter per mother centriole, the process of which requires highly coordinated actions among core factors and modulators. Protein phosphorylation is shown to regulate the stability, localization and activity of centrosome proteins. Here, we report the function of Casein kinase II (CK2) in early Caenorhabditis elegans embryos. The catalytic subunit (KIN-3/CK2α) of CK2 localizes to nuclei, centrosomes and midbodies. Inactivating CK2 leads to cell division defects, including chromosome missegregation, cytokinesis failure and aberrant centrosome behavior. Furthermore, depletion or inhibiting kinase activity of CK2 results in elevated ZYG-1 levels at centrosomes, restoring centrosome duplication and embryonic viability to zyg-1 mutants. Our data suggest that CK2 functions in cell division and negatively regulates centrosome duplication in a kinase-dependent manner

ATX-2, the <i>C</i>. <i>elegans</i> Ortholog of Human Ataxin-2, Regulates Centrosome Size and Microtubule Dynamics

<div><p>Centrosomes are critical sites for orchestrating microtubule dynamics, and exhibit dynamic changes in size during the cell cycle. As cells progress to mitosis, centrosomes recruit more microtubules (MT) to form mitotic bipolar spindles that ensure proper chromosome segregation. We report a new role for ATX-2, a <i>C</i>. <i>elegans</i> ortholog of Human Ataxin-2, in regulating centrosome size and MT dynamics. ATX-2, an RNA-binding protein, forms a complex with SZY-20 in an RNA-independent fashion. Depleting ATX-2 results in embryonic lethality and cytokinesis failure, and restores centrosome duplication to <i>zyg-1</i> mutants. In this pathway, SZY-20 promotes ATX-2 abundance, which inversely correlates with centrosome size. Centrosomes depleted of ATX-2 exhibit elevated levels of centrosome factors (ZYG-1, SPD-5, γ-Tubulin), increasing MT nucleating activity but impeding MT growth. We show that ATX-2 influences MT behavior through γ-Tubulin at the centrosome. Our data suggest that RNA-binding proteins play an active role in controlling MT dynamics and provide insight into the control of proper centrosome size and MT dynamics.</p></div

Knockdown of <i>atx-2</i> enhances levels of PCM factors at centrosomes.

<p>(A) <i>atx-2</i> embryos show increased centrosomal SPD-5 levels at the first metaphase. (B) Relative fluorescence intensity of centrosomal (CE) and cytoplasmic (Cyto) SPD-5 (**<i>p<</i>0.001). (C) Still images from time-lapse movies of embryos expressing mCherry<i>-</i>γ<i>-</i>Tubulin [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1006370#pgen.1006370.ref048" target="_blank">48</a>] and GFP-α-Tubulin. Insets illustrate centrosomes magnified in 3-fold. (D) Measurements of fluorescence intensity of centrosomal and cytoplasmic γ-Tubulin at the first metaphase. Error bars are SD. (***<i>p</i><0.0001; * <i>p</i>>0.005). Bar, 5 μm. (E) Quantitative immunoblot analysis using embryonic lysates reveals no significant changes in overall expression levels of γ-Tubulin (1.01 ± 0.1, n = 10) in <i>atx-2</i> mutant embryos compared to <i>N2</i> control grown at 22°C. α-Tubulin was used as loading control.</p