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IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism
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| Zeitschriftentitel: | Journal of Cell Biology |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , |
| In: | Journal of Cell Biology, 196, 2012, 4, S. 497-511 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Rockefeller University Press
|
| Schlagwörter: |
| author_facet |
Bakkar, Nadine Ladner, Katherine Canan, Benjamin D. Liyanarachchi, Sandya Bal, Naresh C. Pant, Meghna Periasamy, Muthu Li, Qiutang Janssen, Paul M.L. Guttridge, Denis C. Bakkar, Nadine Ladner, Katherine Canan, Benjamin D. Liyanarachchi, Sandya Bal, Naresh C. Pant, Meghna Periasamy, Muthu Li, Qiutang Janssen, Paul M.L. Guttridge, Denis C. |
|---|---|
| author |
Bakkar, Nadine Ladner, Katherine Canan, Benjamin D. Liyanarachchi, Sandya Bal, Naresh C. Pant, Meghna Periasamy, Muthu Li, Qiutang Janssen, Paul M.L. Guttridge, Denis C. |
| spellingShingle |
Bakkar, Nadine Ladner, Katherine Canan, Benjamin D. Liyanarachchi, Sandya Bal, Naresh C. Pant, Meghna Periasamy, Muthu Li, Qiutang Janssen, Paul M.L. Guttridge, Denis C. Journal of Cell Biology IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism Cell Biology |
| author_sort |
bakkar, nadine |
| spelling |
Bakkar, Nadine Ladner, Katherine Canan, Benjamin D. Liyanarachchi, Sandya Bal, Naresh C. Pant, Meghna Periasamy, Muthu Li, Qiutang Janssen, Paul M.L. Guttridge, Denis C. 1540-8140 0021-9525 Rockefeller University Press Cell Biology http://dx.doi.org/10.1083/jcb.201108118 <jats:p>Although the physiological basis of canonical or classical IκB kinase β (IKKβ)–nuclear factor κB (NF-κB) signaling pathway is well established, how alternative NF-κB signaling functions beyond its role in lymphoid development remains unclear. In particular, alternative NF-κB signaling has been linked with cellular metabolism, but this relationship is poorly understood. In this study, we show that mice deleted for the alternative NF-κB components IKKα or RelB have reduced mitochondrial content and function. Conversely, expressing alternative, but not classical, NF-κB pathway components in skeletal muscle stimulates mitochondrial biogenesis and specifies slow twitch fibers, suggesting that oxidative metabolism in muscle is selectively controlled by the alternative pathway. The alternative NF-κB pathway mediates this specificity by direct transcriptional activation of the mitochondrial regulator PPAR-γ coactivator 1β (PGC-1β) but not PGC-1α. Regulation of PGC-1β by IKKα/RelB also is mammalian target of rapamycin (mTOR) dependent, highlighting a cross talk between mTOR and NF-κB in muscle metabolism. Together, these data provide insight on PGC-1β regulation during skeletal myogenesis and reveal a unique function of alternative NF-κB signaling in promoting an oxidative metabolic phenotype.</jats:p> IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism Journal of Cell Biology |
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| title |
IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism |
| title_unstemmed |
IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism |
| title_full |
IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism |
| title_fullStr |
IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism |
| title_full_unstemmed |
IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism |
| title_short |
IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism |
| title_sort |
ikkα and alternative nf-κb regulate pgc-1β to promote oxidative muscle metabolism |
| topic |
Cell Biology |
| url |
http://dx.doi.org/10.1083/jcb.201108118 |
| publishDate |
2012 |
| physical |
497-511 |
| description |
<jats:p>Although the physiological basis of canonical or classical IκB kinase β (IKKβ)–nuclear factor κB (NF-κB) signaling pathway is well established, how alternative NF-κB signaling functions beyond its role in lymphoid development remains unclear. In particular, alternative NF-κB signaling has been linked with cellular metabolism, but this relationship is poorly understood. In this study, we show that mice deleted for the alternative NF-κB components IKKα or RelB have reduced mitochondrial content and function. Conversely, expressing alternative, but not classical, NF-κB pathway components in skeletal muscle stimulates mitochondrial biogenesis and specifies slow twitch fibers, suggesting that oxidative metabolism in muscle is selectively controlled by the alternative pathway. The alternative NF-κB pathway mediates this specificity by direct transcriptional activation of the mitochondrial regulator PPAR-γ coactivator 1β (PGC-1β) but not PGC-1α. Regulation of PGC-1β by IKKα/RelB also is mammalian target of rapamycin (mTOR) dependent, highlighting a cross talk between mTOR and NF-κB in muscle metabolism. Together, these data provide insight on PGC-1β regulation during skeletal myogenesis and reveal a unique function of alternative NF-κB signaling in promoting an oxidative metabolic phenotype.</jats:p> |
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| author | Bakkar, Nadine, Ladner, Katherine, Canan, Benjamin D., Liyanarachchi, Sandya, Bal, Naresh C., Pant, Meghna, Periasamy, Muthu, Li, Qiutang, Janssen, Paul M.L., Guttridge, Denis C. |
| author_facet | Bakkar, Nadine, Ladner, Katherine, Canan, Benjamin D., Liyanarachchi, Sandya, Bal, Naresh C., Pant, Meghna, Periasamy, Muthu, Li, Qiutang, Janssen, Paul M.L., Guttridge, Denis C., Bakkar, Nadine, Ladner, Katherine, Canan, Benjamin D., Liyanarachchi, Sandya, Bal, Naresh C., Pant, Meghna, Periasamy, Muthu, Li, Qiutang, Janssen, Paul M.L., Guttridge, Denis C. |
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| container_title | Journal of Cell Biology |
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| description | <jats:p>Although the physiological basis of canonical or classical IκB kinase β (IKKβ)–nuclear factor κB (NF-κB) signaling pathway is well established, how alternative NF-κB signaling functions beyond its role in lymphoid development remains unclear. In particular, alternative NF-κB signaling has been linked with cellular metabolism, but this relationship is poorly understood. In this study, we show that mice deleted for the alternative NF-κB components IKKα or RelB have reduced mitochondrial content and function. Conversely, expressing alternative, but not classical, NF-κB pathway components in skeletal muscle stimulates mitochondrial biogenesis and specifies slow twitch fibers, suggesting that oxidative metabolism in muscle is selectively controlled by the alternative pathway. The alternative NF-κB pathway mediates this specificity by direct transcriptional activation of the mitochondrial regulator PPAR-γ coactivator 1β (PGC-1β) but not PGC-1α. Regulation of PGC-1β by IKKα/RelB also is mammalian target of rapamycin (mTOR) dependent, highlighting a cross talk between mTOR and NF-κB in muscle metabolism. Together, these data provide insight on PGC-1β regulation during skeletal myogenesis and reveal a unique function of alternative NF-κB signaling in promoting an oxidative metabolic phenotype.</jats:p> |
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| imprint_str_mv | Rockefeller University Press, 2012 |
| institution | DE-D161, DE-Zwi2, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1 |
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| physical | 497-511 |
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| spelling | Bakkar, Nadine Ladner, Katherine Canan, Benjamin D. Liyanarachchi, Sandya Bal, Naresh C. Pant, Meghna Periasamy, Muthu Li, Qiutang Janssen, Paul M.L. Guttridge, Denis C. 1540-8140 0021-9525 Rockefeller University Press Cell Biology http://dx.doi.org/10.1083/jcb.201108118 <jats:p>Although the physiological basis of canonical or classical IκB kinase β (IKKβ)–nuclear factor κB (NF-κB) signaling pathway is well established, how alternative NF-κB signaling functions beyond its role in lymphoid development remains unclear. In particular, alternative NF-κB signaling has been linked with cellular metabolism, but this relationship is poorly understood. In this study, we show that mice deleted for the alternative NF-κB components IKKα or RelB have reduced mitochondrial content and function. Conversely, expressing alternative, but not classical, NF-κB pathway components in skeletal muscle stimulates mitochondrial biogenesis and specifies slow twitch fibers, suggesting that oxidative metabolism in muscle is selectively controlled by the alternative pathway. The alternative NF-κB pathway mediates this specificity by direct transcriptional activation of the mitochondrial regulator PPAR-γ coactivator 1β (PGC-1β) but not PGC-1α. Regulation of PGC-1β by IKKα/RelB also is mammalian target of rapamycin (mTOR) dependent, highlighting a cross talk between mTOR and NF-κB in muscle metabolism. Together, these data provide insight on PGC-1β regulation during skeletal myogenesis and reveal a unique function of alternative NF-κB signaling in promoting an oxidative metabolic phenotype.</jats:p> IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism Journal of Cell Biology |
| spellingShingle | Bakkar, Nadine, Ladner, Katherine, Canan, Benjamin D., Liyanarachchi, Sandya, Bal, Naresh C., Pant, Meghna, Periasamy, Muthu, Li, Qiutang, Janssen, Paul M.L., Guttridge, Denis C., Journal of Cell Biology, IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism, Cell Biology |
| title | IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism |
| title_full | IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism |
| title_fullStr | IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism |
| title_full_unstemmed | IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism |
| title_short | IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism |
| title_sort | ikkα and alternative nf-κb regulate pgc-1β to promote oxidative muscle metabolism |
| title_unstemmed | IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism |
| topic | Cell Biology |
| url | http://dx.doi.org/10.1083/jcb.201108118 |