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Human mitochondrial mRNAs are stabilized with polyadenylation regulated by mitochondria-specific poly(A) polymerase

Takashi Nagaike1, Tsutomu Suzuki, Takayuki Katoh

  • 1Department of Medical Genome Sciences, Graduate School of Frontier Sciences, University of Tokyo, Kashiwa, Chiba Prefecture, Japan.

The Journal of Biological Chemistry
|March 17, 2005
PubMed

Insights

Human mitochondrial poly(A) polymerase (PAP) controls mRNA polyadenylation, crucial for mitochondrial gene expression and function. Its inactivation shortens poly(A) tails, impacting mRNA stability and cellular respiration.

Area of Science:

  • Mitochondrial biology
  • Gene expression regulation
  • Molecular genetics

Background:

  • Mammalian mitochondrial mRNAs possess short 3' poly(A) tails synthesized by mitochondrial poly(A) polymerase (PAP).
  • Polyadenylation is essential for forming UAA stop codons and tRNA maturation.
  • The functional roles of poly(A) tails in mitochondrial mRNA translation and turnover remain largely unelucidated.

Purpose of the Study:

  • To investigate the roles of human mitochondrial PAP (hmtPAP) and human polynucleotide phosphorylase (hPNPase) in controlling mitochondrial mRNA poly(A) synthesis.
  • To elucidate the functional significance of poly(A) tail length in mitochondrial gene expression and cellular respiration.

Main Methods:

  • RNA interference (RNAi) using small interfering RNA (siRNA) to partially inactivate hmtPAP in HeLa cells.
  • Analysis of poly(A) tail lengths, steady-state mRNA levels, and translational products.
  • Measurement of mitochondrial membrane potential and oxygen consumption.

Main Results:

  • Partial inactivation of hmtPAP led to shortened poly(A) tails, decreased steady-state levels of specific mitochondrial mRNAs, and reduced translational products.
  • Knockdown of hmtPAP resulted in defective mitochondrial membrane potentials and diminished oxygen consumption.
  • Knockdown of hPNPase caused significantly extended poly(A) tails on mitochondrial mRNAs.

Conclusions:

  • The poly(A) length of human mitochondrial mRNAs is regulated by hmtPAP-mediated polyadenylation and hPNPase-mediated deadenylation.
  • Polyadenylation is essential for the stability of mitochondrial mRNAs.
  • Mitochondrial mRNA polyadenylation plays a critical role in maintaining mitochondrial function, including membrane potential and cellular respiration.

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