Developing programme leadership in an Australian university: An institutional approach to professional learning and development

Academic programme leadership in universities is pivotal in fulfilling the institution’s purpose of offering quality educational experiences for students (Stensaker et al, 2018). Our chapter describes the Building Program Leadership Strategy designed and enacted at Griffith University during 2014–2018 that aimed to develop programme leadership through facilitating a coordinated, university-wide, systems-based approach to academic professional learning and organisational development. At Griffiths those that lead programmes of study are ‘Programme Directors’, in keeping with this edition we use the term ‘pro gramme leader’ (PL) throughout. Initially, we will provide a brief overview of our institutional context, before describing the strategy, focusing particularly on the professional learning approaches and activities developed and facilitated. We will then provide the findings of our participatory action research study, and share key learnings in relation to how the strategy influenced a shift in perceptions and practices of programme leadership by individual PLs and teams, along with the valuing of programme leadership by the wider University system.

Case Study 1: Developing a role statement for programme leadership

This case-study describes the collaborative development and evolution of Griffith University's Program Director's role statement and in particular the representation of the change nature of the role's leadership orientation as evident in its various iterations

Dataset 2.tar

Zipped; raw ABI sequence data files

The Mutation <i>cyd vicious</i> Displays Neural Crest and Eye Defects

<p>Brightfield images of stage ~38 outcrossed sibling wild-type embryo (A) and gynogenetic <i>cyd</i> embryo (B). Likely neural crest–derived pigmented cells (arrows, [C] and [D]) fail to migrate in <i>cyd</i>, and instead populate the lumen of the neural tube. St. 40 wild-type eye (E) displays laminar organization surrounded by prominent pigmented epithelium. <i>cyd</i> eyes form a poorly laminated ball of neural retina surrounding a central mass of pigmented tissue, and no lens tissue is visible (F).</p

Axis Extension Mutations

<p>The dwarf phenotypes <i>tansoku</i>, <i>yodaa</i>, and <i>issunboushi</i> show relatively normal head and trunk structures, but are defective in tail extension. Anti-laminin immunohistochemistry reveals discrete defects in axial structures, with <i>tansoku</i> ([C] and [D]) displaying a reduced number of relatively well-ordered somites, <i>issunboushi</i> ([G] and [H]) showing highly disordered intersomitic boundaries, and <i>yodaa</i> ([E] and [F]) displaying an intermediate phenotype.</p

Mutation Detection

<p>All sequences generated by TILLING (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020091#pgen-0020091-g007" target="_blank">Figure 7</a>) are examined and compared to a reference sequence by a Mutation Finder program. Any disparities with reference sequences are recorded for view in a Mutation Display window (A). Reference DNA and amino acid sequence is displayed above the trace and the TILLING trace below. Boxes around reference sequence nucleotides denote alterations in one or more TILLING traces; box color indicates number of traces altered. The asterisk above the reference amino acid sequence designates a position at which a mutation has been visually confirmed and recorded. Clicking on a box or asterisk will recover the trace(s) containing the change. Traces that are not confirmed are dismissed. All processed traces are accessible via the pull down trace lists. Examples of mutations are displayed for silent, missense, and nonsense alongside wild-type traces for comparison (B).</p

Reverse Screen Strategy

<p>ENU-treated sperm (G0) was used to fertilize wild-type eggs (in vitro fertilization), and the resulting F1 families raised to adulthood. F1 males were killed and their testes dissociated, with a portion used to generate F2 tadpoles and the remainder frozen in several aliquots per individual (F1 library). F1 females were used in the gynogenetic forward screens (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020091#pgen-0020091-g001" target="_blank">Figure 1</a>). F2 genomic DNA was isolated from the tadpoles for reverse genetic (TILLING) screens. Known genomic sequences were used to design nested PCR primers, and then individual F2 tadpole amplicons were sequenced to detect induced mutations. Mutations are then recovered from frozen testes by in vitro fertilization for subsequent phenotypic analysis.</p

Phenotypes Detected

<p>Defects were sorted into ten broad categories (shown with representative images): eye <i>(zatoichi),</i> inner ear and otolith <i>(komimi),</i> neural crest/pigment <i>(cyd vicious),</i> dwarf <i>(issunboushi),</i> axial <i>(bulldog),</i> circulation <i>(desert tad),</i> gut <i>(haggis),</i> cardiovascular system and motility, and head <i>(troll)</i>. Color code (green, orange, red) is described in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020091#pgen-0020091-g001" target="_blank">Figure 1</a> and used in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020091#pgen-0020091-t002" target="_blank">Tables 2</a> and <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020091#pgen-0020091-t003" target="_blank">3</a> to denote current confirmation status of individual mutations in the pipeline. Provisional alleles (“prov,” green) have not yet been assayed for heritability.</p

Forward Screen Strategy

<p>Following ENU mutagenesis of postmeiotic sperm and fertilization of wild-type eggs, a founder F1 generation was raised. Males were used in a reverse genetic strategy (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020091#pgen-0020091-g007" target="_blank">Figure 7</a>). F1 females were used to generate gynogenetic embryos that were screened for embryonic defects. F1 females carrying defects were outcrossed and the resulting F2 embryos screened for carriers, then sibling intercrossed. Color code indicates status of specific mutations (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020091#pgen-0020091-g002" target="_blank">Figure 2</a> and <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020091#pgen-0020091-t002" target="_blank">Tables 2</a> and <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020091#pgen-0020091-t003" target="_blank">3</a>): red for phenotypes confirmed in the progeny of a conventional F2 sibling intercross, orange for phenotypes confirmed heritable by backcross or F2 gynogenesis, green for phenotypes observed twice from gynogenesis of an individual F1 female, and blue for phenotypes observed once and not yet retested.</p

<i>wha</i> Embryos Show Defects in Hematopoeisis

<p>Whole mount in situ hybridization with α-globin suggests that <i>wha</i> blood distribution is aberrant ([A] and [C]), with reduced globin staining pooled ventrally (black arrows) rather than distributed throughout the circulatory system as in wild-type tadpoles. Comparison of ventral views of <i>wha</i> (C) globin staining with that of <i>muzak</i> (B), a mutant which is impaired in heart function but not hematopoiesis, leading to ventral pooling of normal levels of blood (white arrows), confirms that <i>wha</i> is quantitatively defective in blood formation rather than circulation. See also <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020091#pgen-0020091-t006" target="_blank">Tables 6</a> and <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020091#pgen-0020091-t007" target="_blank">7</a> for microarray analysis of <i>wha.</i></p