TFAM mislocalization during spermatogenesis

Sam Kavoosi; Martin Picard; Brett A Kaufman

doi:10.1016/j.tig.2023.11.002

TFAM mislocalization during spermatogenesis

Trends Genet. 2024 Feb;40(2):112-114. doi: 10.1016/j.tig.2023.11.002. Epub 2023 Nov 29.

Authors

Sam Kavoosi¹, Martin Picard², Brett A Kaufman³

Affiliations

¹ Center for Metabolism and Mitochondrial Medicine, Vascular Medicine Institute, Division of Cardiology, University of Pittsburgh School of Medicine, 200 Lothrop St. BST W1044, Pittsburgh, PA 15261, USA.
² Division of Behavioral Medicine, Department of Psychiatry, Houston Merritt Center, Columbia Translational Neuroscience Initiative, Columbia University Irving Medical Center, New York, NY 10032, USA; Department of Neurology, H. Houston Merritt Center, Columbia Translational Neuroscience Initiative, Columbia University Irving Medical Center, New York, NY 10032, USA.
³ Center for Metabolism and Mitochondrial Medicine, Vascular Medicine Institute, Division of Cardiology, University of Pittsburgh School of Medicine, 200 Lothrop St. BST W1044, Pittsburgh, PA 15261, USA. Electronic address: bkauf@pitt.edu.

PMID: 38036338
DOI: 10.1016/j.tig.2023.11.002

Abstract

Mitochondrial DNA (mtDNA) is inherited almost exclusively from the maternal lineage. Paternal destruction of either mtDNA or whole mitochondria has been the dominant model for mtDNA transmission. Recently, Lee et al. provided evidence for mitochondrial transcription factor A (TFAM) import sequence regulation as a potential cause for mtDNA depletion in human sperm before fertilization.

Keywords: TFAM; mtDNA; spermatogenesis; uniparental inheritance.

MeSH terms

DNA, Mitochondrial / genetics
DNA-Binding Proteins / metabolism
Humans
Male
Mitochondria / genetics
Mitochondrial Proteins / genetics
Semen*
Spermatogenesis* / genetics
Spermatozoa / metabolism
Transcription Factors / metabolism

Substances

DNA, Mitochondrial
Mitochondrial Proteins
TFAM protein, human
DNA-Binding Proteins
Transcription Factors