Zubryckis point: Amongst Equals, utilitarian film in the Australian labour movement

A film history project on the Australian trade union movement commissioned in the late 1980s for Australias bicentennial year, 1988, came to grief over differing views of the labour movements past and contention around the rights and ethics of the filmmaker when a work is commissioned or sponsored. In the political context of the late 1980s there had been a decade of collaboration between trade unions and artists, but in this case filmmaker Tom Zubrycki was caught in a web of intrigue and complex agendas as he sought to complete this sponsored film. Zubrycki challenged the Australian Council of Trade Unions (ACTU) for the right to finish and distribute Amongst Equals, but without success. The struggle to resolve the Amongst Equals dispute continued for years and flared into a heated public debate. This case study illustrates dilemmas facing the artist, historian or filmmaker making sponsored work. A feature-length version of the unfinished film, not seen since 1991with inter-titles identifying scenes that the ACTU wanted revised or deleted was screened by Melbourne Cinematheque in October 2018, marking 30 years since the Australian bicentennial

Training and aging modulate the loss-of-balance phenotype observed in a new ENU-induced allele of Otopetrin1

International audienceBACKGROUND INFORMATION: The sensing of head movement in mammals depends upon the vestibular endorgan of the inner ear, a complex structure made up of the semicircular canals and otoliths. Due to the similarity between the human and mouse vestibular apparatus, the analysis of mutant mouse is a valuable strategy aiming to identify genes involved in the control of balance and movement. RESULTS: In the course of a genome-wide chemical-mutagenesis programme, we isolated a recessive mutation, named ied (inner ear defect), which induced a severe loss-of-balance. A detailed phenotypic analysis of the mutant mice demonstrates that the balance impairment does not affect the motor activity and can be rescued, in part, by training, despite a complete agenesis of otoconia in the utricule and the saccule of the inner ear. Molecular characterization of the ied mutation revealed a transversion that affects the splicing of the second exon of the Otopetrin1 gene located on mouse chromosome 5. The consequence of such a mutation leads to a disruption of the transcription of the gene. CONCLUSIONS: The identification of the ied knock-down allele strengthens the role of the Otopetrin1 in the sensing of balance. Moreover, the rescue of the ied mutant phenotype in specific behavioural tasks confirmed that other sensory inputs or neural plasticity can compensate, to some extent, for the loss-of-balance. In the future, the ied mutant mice might be helpful to study the genetic control of the compensation strategies developed by organisms to counteract balance defects