1. |
- Niemi, MEK, et al.
(author)
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- 2021
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swepub:Mat__t
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2. |
- Kanai, M, et al.
(author)
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- 2023
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swepub:Mat__t
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3. |
- Stroud, J.T., et al.
(author)
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Priority effects transcend scales and disciplines in biology
- 2024
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In: Trends in Ecology & Evolution. - : Elsevier. - 0169-5347 .- 1872-8383.
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Research review (peer-reviewed)abstract
- Although primarily studied through the lens of community ecology, phenomena consistent with priority effects appear to be widespread across many different scenarios spanning a broad range of spatial, temporal, and biological scales. However, communication between these research fields is inconsistent and has resulted in a fragmented co-citation landscape, likely due to the diversity of terms used to refer to priority effects across these fields. We review these related terms, and the biological contexts in which they are used, to facilitate greater cross-disciplinary cohesion in research on priority effects. In breaking down these semantic barriers, we aim to provide a framework to better understand the conditions and mechanisms of priority effects, and their consequences across spatial and temporal scales.
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4. |
- Van Haute, L., et al.
(author)
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TEFM variants impair mitochondrial transcription causing childhood-onset neurological disease
- 2023
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In: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 14:1
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Journal article (peer-reviewed)abstract
- Mutations in the mitochondrial or nuclear genomes are associated with a diverse group of human disorders characterized by impaired mitochondrial respiration. Within this group, an increasing number of mutations have been identified in nuclear genes involved in mitochondrial RNA biology. The TEFM gene encodes the mitochondrial transcription elongation factor responsible for enhancing the processivity of mitochondrial RNA polymerase, POLRMT. We report for the first time that TEFM variants are associated with mitochondrial respiratory chain deficiency and a wide range of clinical presentations including mitochondrial myopathy with a treatable neuromuscular transmission defect. Mechanistically, we show muscle and primary fibroblasts from the affected individuals have reduced levels of promoter distal mitochondrial RNA transcripts. Finally, tefm knockdown in zebrafish embryos resulted in neuromuscular junction abnormalities and abnormal mitochondrial function, strengthening the genotype-phenotype correlation. Our study highlights that TEFM regulates mitochondrial transcription elongation and its defect results in variable, tissue-specific neurological and neuromuscular symptoms.
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