Skip to main content
padlock icon - secure page this page is secure

Free Content A peroxisomal carrier delivers NAD+ and contributes to optimal fatty acid degradation during storage oil mobilization

Download Article:

You have access to the full text article on a website external to Ingenta Connect.

Please click here to view this article on Wiley Online Library.

You may be required to register and activate access on Wiley Online Library before you can obtain the full text. If you have any queries please visit Wiley Online Library


The existence of a transport protein that imports cytosolic NAD+ into peroxisomes has been controversially discussed for decades. Nevertheless, the biosynthesis of NAD+ in the cytosol necessitates the import of NAD+ into peroxisomes for numerous reduction/oxidation (redox) reactions. However, a gene encoding such a transport system has not yet been identified in any eukaryotic organism. Here, we describe the peroxisomal NAD+ carrier in Arabidopsis. Our candidate gene At2g39970 encodes for a member of the mitochondrial carrier family. We confirmed its peroxisomal localization using fluorescence microscopy. For a long time At2g39970 was assumed to represent the peroxisomal ATP transporter. In this study, we could show that the recombinant protein mediated the transport of NAD+. Hence, At2g39970 was named PXN for peroxisomal NAD+ carrier. The loss of PXN in Arabidopsis causes defects in NAD+‐dependent β‐oxidation during seedling establishment. The breakdown of fatty acid released from storage oil was delayed, which led to the retention of oil bodies in pxn mutant seedlings. Based on our results, we propose that PXN delivers NAD+ for optimal fatty acid degradation during storage oil mobilization.
No References
No Citations
No Supplementary Data
No Article Media
No Metrics

Document Type: Research Article

Affiliations: Institut für Biochemie der Pflanzen, Heinrich-Heine Universität Düsseldorf, 40225 Düsseldorf, Germany

Publication date: January 1, 2012

  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more