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Fig. 3. Ate1 knockout results in defects in the sarcomeric structure of
cardiac myofibrils. (A) Wild-type sarcomere illustrating parameters
measured. (B) Frequency distribution of sarcomere length and Z-band
thickness in wild-type (WT) and knockout (KO) mouse hearts at E12.5 (E12) and
E14.5 (E14). In wild-type and mutant E12.5 hearts, both sarcomere length and
Z-band thickness are relatively constant, with small variations due to
differences in the contractile state of individual myocytes. In knockout
hearts at later stages (E14.5), the frequency distribution of both parameters
becomes wider, suggesting disorganization of the sarcomeres.
(C,D) Defects in Z-band thickness (C) and sarcomere length (D).
Average sarcomere lengths (± s.d.) were 1389 ± 141 nm (WT E12,
n=27), 1490 ± 101 nm (KO E12, n=39), 1682 ±
116 (WT E14, n=116) and 1179 ± 199 (KO E14, n=124).
Average Z-band thicknesses were 86 ± 19 nm (WT E12, n=27), 87
± 23 nm (KO E12, n=39), 120 ± 23 (WT E14,
n=116) and 142 ± 36 (KO E14, n=124). (E)
Examples of other defects in myofibril structure seen in Ate1
knockout hearts, including myofibril branching at Z-bands and asymmetric
sarcomeres, in which the density of the filaments on the two sides is markedly
different. Scale bars: 500 nm.
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