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Investigating Abnormal Chromosome Tolerance in Wild Yeast Cells

Hose et al (2020) researched the genetic basis of aneuploidy tolerance in wild yeast in a recent edition of Elife.

Aneuploidy, or the abnormal chromosome numbers in a cell, is a harmful condition in developmental stages of wild yeast, yet is also common in plant cancers and pathogenic fungi. It is interesting to note that aneuploidy tolerance varies; for instance, researchers found that some wild isolates of baker’s yeast can tolerate chromosome amplification, while laboratory strains cannot. 

To study the genetic basis of how well wild yeast can tolerate aneuploidy, researchers mapped the genetic basis to Ssd1, an RNA-binding translational regulator that functions in wild strains but is defective in a laboratory strain “W303.” 

Researchers found that aneuploidy tolerance is enabled via a role for Ssd1 in mitochondrial physiology, such as binding and regulating nuclear-encoded mitochondrial mRNAs.

Transgenic animal models demonstrate that mice have similar COPD-related skeletal muscle dysfunction as humans

Balnis et al (2020) recently studied the mechanisms of COPD-related skeletal muscle dysfunction using an established transgenic animal model of COPD in a recently published paper in the Journal of Applied Physiology. 

Patients with chronic obstructive pulmonary disease (COPD), a disease that is characterized by obstructed airflow to the lungs and is associated with long-term exposure to cigarette smoke, often also develop skeletal muscle dysfunction. Overall, the comorbidity of COPD and skeletal muscle dysfunction is associated with outcomes such as poor health and mortality.

While some research has suggested that skeletal muscle dysfunction may be the result of COPD-related conditions, such as protein degradation and metabolic disruption, there is still poor understanding on what mechanisms would regulate these processes, as there is little to no research on a validated animal model of pulmonary emphysema. Therefore, Balnis et al (2020) sought to use such a model based on inducible UL-13-driven pulmonary emphysema (IL-13TG) to study the mechanisms of skeletal muscle dysfunction.

Using a transgenic mouse model, researchers found that the skeletal muscles of emphysematous mice are similar to those developed by human patients with COPD. For instance, both groups develop muscular atrophy and have decreased oxygen consumption. Within skeletal muscles, both groups also had downregulated ATP binding and bioenergetics.

Researchers concluded that transgenic animal models of COPD are useful to understand skeletal-muscle dysfunction in humans.