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Ultrastruct Pathol. 2015;39(5):336-9. doi: 10.3109/01913123.2015.1042610. Epub 2015 Jun 25.

Megamitochondria in Cardiomyocytes of a Knockout (Klf15-/-) Mouse.

Author information

1
a Department of Biological Sciences , School of Dental Medicine, Case Western Reserve University , Cleveland , OH , USA .
2
b Center for Mitochondrial Disease, School of Medicine, Case Western Reserve University , Cleveland , OH , USA .
3
c Electron Microscopy Facility, School of Medicine, Case Western Reserve University , Cleveland , OH , USA .
4
d Departments of Pharmacology and of Medicine , School of Medicine, Case Western Reserve University , Cleveland , OH , USA .
5
e Case Cardiovascular Research Institute, School of Medicine, Case Western Reserve University , Cleveland , OH , USA , and.
6
f Harrington Heart & Vascular Institute, University Hospitals Case Medical Center , Cleveland , OH , USA.

Abstract

The Kruppel-like factors (KLF) family of zinc-finger transcriptional regulators control many aspects of cardiomyocyte structure and function. Deletion of Klf15 from the nuclear genome in mice affects cardiac mitochondria. Some become grossly enlarged, extending many sarcomeres in length. These display many sites of incipient pinching, but there is little attenuation of the megamitochondria at these sites; there are no examples of organelles that clearly have reached the point where further membrane encroachment will cause separation into smaller daughter mitochondria. It is clear that deletion of Klf15 interferes with nuclear control of mitochondrial fission, whereas fusion appears to be unaffected.

KEYWORDS:

Cardiac mitochondria; kruppel-like factor (KLF); megamitochondria; mitochondrial fission; mitochondrial fusion

PMID:
26111268
PMCID:
PMC4827860
DOI:
10.3109/01913123.2015.1042610
[Indexed for MEDLINE]
Free PMC Article

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