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Glover, E.

Publications and source records attributed to Glover, E..

3 recordsLinked to original sources

Intercellular mitochondrial transfer and transmitophagy in response to protein import dysfunction

Mitochondrial protein import is critical for organelle biogenesis and maintenance, essential processes for cellular homeostasis. Import dysfunction compromises cellular energy supplies which is damaging to cells, particularly those with high energetic demands like neurons. Previously, we have shown that import failure is rescued by intercellular mitochondrial transfer via tunnelling nanotubes (TNTs) however, the fate of the transferred mitochondria and the mechanistic basis for rescue was unresolved. Here, we show that bi-directional mitochondrial trafficking between cells harbouring import-defective and import-competent mitochondria has distinct regulation and consequences. Transferred import-defective mitochondria are highly fragmented and destined for canonical lysosomal degradation. In contrast, ROS-producing mitochondria at the periphery of cells with import-competent mitochondria are transferred into neighbouring cells undergoing import failure; these new arrivals then accumulate within previously uncharacterised mitochondrial degradation bodies (MBDs). We speculate that the co-operation of these distinct examples of TNT- mediated conventional and non-canonical transmitophagy instigate mitochondrial regeneration, and thereby rescue.

cell biology↗

Low effective population size but high heterozygosity revealed by SNP analyses in adult and juvenile Thuja plicata in UK Woodlands

Thuja plicata is a conifer tree that is appreciated for its cultural, ecological and wood quality features in its natural range in western North America. It is also used in Europe and the UK for timber production. Some T. Plicata plantations in the UK are converted to Continuous Cover Forestry (CCF) management which uses natural regeneration and concerns have been raised about the genetic diversity in both the adult trees and the offspring. We studied species diversity, stand structure, and genetic diversity in four UK woodlands planted with T. plicata which contained both adults and naturally regenerated individuals. We discovered 61,104 Single Nucleotide Polymorphisms (SNPs) using Genotyping-by-Sequencing (GBS) and retained 504 SNPs for analysis. We selected 67 SNPs for PCR-based genotyping of 163 adults and 176 juveniles. We found a large number of monomorphic sites (40.3%) most of which were restricted to adults in a single woodland, indicative of a high genetic differentiation among woodlands. The effective population size (Ne) was very low across all sites (Ne < 100), varied between adults and juveniles, and was lowest in the most diverse woodland in terms of species and structure. In contrast, heterozygosity was high overall (Ho = 0.38), except in the divergent woodland (Ho = 0.26), and did not vary between adults and juveniles. Our findings and genotyping methods provide insights into the ability of CCF-managed woodlands, including instances of low genetic diversity in T. plicata, to face environmental shifts and disease threats.

genomics↗

Intercellular Mitochondrial Transfer as a Rescue Mechanism in Response to Protein Import Failure

Mitochondria are the powerhouses of eukaryotic cells, composed mostly of nuclear-encoded proteins imported from the cytosol. Thus, problems with the import machinery will disrupt their regenerative capacity and the cells energy (ATP) supplies-particularly troublesome for energy demanding cells like neurons and myocytes. Unsurprisingly then, dysfunctional import is implicated in disease. This study explores the consequences of import failure in mammalian cells; wherein, blocking the import machinery has profound effects on mitochondrial ultra-structure and dynamics, but, surprisingly, does not impact import. The explanation is an astonishing response involving intercellular mitochondrial transfer via tunnelling nanotubes: for the import of healthy mitochondria and jettisoning of those with jammed import sites. These observations support the existence of a widespread mechanism for the rescue of mitochondrial protein import failure. One-Sentence SummaryA mitochondrial import rescue mechanism involving intercellular mitochondrial transport through tunneling nanotubes (TNTs).

cell biology↗