Mitochondria have long been the Rodney Dangerfield of cellular
organelles. Believed to be the remnants of bacterial infection of
eukaryotic cells eons ago, the mitochondrion evolved a symbiotic
relationship in which it dutifully served as the efficient source
of A TP for cell function. The extraordinary dependence of cells on
the energy provided by mito chondrial oxidative metabolism of
glucose, especially through critical organs such as the heart and
brain, is underlined by the fatal consequences of toxins that
interfere with the mitochondrial electron transport system.
Consistent with their ancestry, the mitochondria have their own DNA
that encodes many but not all of their proteins. The mitochon dria
and their genes come from the mother via the ovum since sperm do
not possess mitochondria. This extranuclear form of inheritance
derived exclusively from the female side has proven to be a
powerful tool for tracing the evolution by the number of base
substitutions in mtDNA. That mitochondrial gene mutations might be
a source of human dis ease became evident a decade ago with the
characterization of a group of multisystem disorders, typically
involving the nervous system, which are transmitted from mother to
child. Specific point mutations in mtDNA have been associated with
the different syndromes.
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