The impact of university STEM assets: A systematic review of the empirical evidence.

BACKGROUND: Innovation ecosystems are an important driver of regional economic growth and development. STEM assets connected to universities may play an important role in such ecosystems. OBJECTIVE: To systematically review the literature relating to the effect of university STEM assets on regional economies and innovation ecosystems, providing a better understanding of how the impact is generated and constrained, as well as identifying any gaps in knowledge. METHODS: Keyword and text word searches using the Web of Science Core Collection (Clarivate), Econlit (EBSCO) and ERIC (EBSCO) were performed in July 2021 and February 2023. Papers were double screened on abstract and title, and were included if there was consensus that they fulfilled the inclusion criteria of: (i) relating to an OECD country; (ii) having been published between 1 January 2010 and 28 February 2023; and (iii) concerning the impact of STEM assets. Data extraction was undertaken for each article by a single reviewer and checked by a second reviewer. Due to the heterogeneity of the study designs and outcome measures used, it was not possible to perform a quantitative synthesis of results. A narrative synthesis was subsequently undertaken. RESULTS: Of the 162 articles identified for detailed review, 34 were accepted as being sufficiently relevant to the study to be included for final analysis. Three important features identified were that the literature: i) is predominately concerned with supporting new businesses; ii) describes a high level of involvement with a university in providing that support; and iii studies economic impacts at local, regional and national levels. DISCUSSION: The evidence points to a gap in the literature relating to looking at the broader impact of STEM assets and any corresponding transformational, system-level effects that go beyond narrowly defined, short to medium-term outcomes. The main limitation of this review is that information on STEM assets in the non-academic literature is not captured.

A cyclin-binding motif in human papillomavirus type 18 (HPV18) E1

The G2/M arrest function of human papillomavirus (HPV) E4 proteins is hypothesized to be necessary for viral genome amplification. Full-length HPV18 E1^E4 protein is essential for efficient viral genome amplification. Here we identify key determinants within a CDK-bipartite consensus recognition motif in HPV18 E1^E4 that are critical for association with active CDK-cyclin complexes and in vitro phosphorylation at the predicted CDK phosphorylation site (threonine 23). The optimal cyclin-binding sequence ((43)RRLL(46)) within this E4 motif is required for G2/M arrest of primary keratinocytes and correlates with cytoplasmic retention of cyclin B1, but not cyclin A. Disruption of this motif in the E4 ORF of HPV18 genomes, and the subsequent generation of stable cell lines in primary keratinocytes revealed that this motif was not essential for viral genome amplification or L1 capsid protein induction. We conclude that the HPV18 E4 G2/M arrest function does not play a role in early vegetative events.

AtMSH5 partners AtMSH4 in the class I meiotic crossover pathway in Arabidopsis thaliana, but is not required for synapsis.

MSH5, a meiosis-specific member of the MutS-homologue family of genes, is required for normal levels of recombination in budding yeast, mouse and Caenorhabditis elegans. In this paper we report the identification and characterization of the Arabidopsis homologue of MSH5 (AtMSH5). Transcripts of AtMSH5 are specific to reproductive tissues, and immunofluorescence studies indicate that expression of the protein is abundant during prophase I of meiosis. In a T-DNA tagged insertional mutant (Atmsh5-1), recombination is reduced to about 13% of wild-type levels. The residual chiasmata are randomly distributed between cells and chromosomes. These data provide further evidence for at least two pathways of meiotic recombination in Arabidopsis and indicate that AtMSH5 protein is required for the formation of class I interference-sensitive crossovers. Localization of AtMSH5 to meiotic chromosomes occurs at leptotene and is dependent on DNA double-strand break formation and strand exchange. Localization of AtMSH5 to the chromatin at mid-prophase I is dependent on expression of AtMSH4. At late zygotene/early pachytene a proportion of AtMSH5 foci co-localize with AtMLH1 which marks crossover-designated sites. Chromosome synapsis appears to proceed normally, without significant delay, in Atmsh5-1 but the pachytene stage is extended by several hours, indicative of the operation of a surveillance system that monitors the progression of prophase I.