Biology 201 B1 Assignment 1

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Biology 201 B1 Assignment #2
A four question analysis on "The myosin-interacting protein SMYD1 is essential for sarcomere organization" by Just et al. (2011)
1.) Wild-type Fla Mutant (SMYD-deficient)

In the current study, the authors used a zebra fish mutant known as Flatline (fla). This mutant contains a nonsense mutation within the SMYD1 gene, consequently, these mutants show disturbed sarcomere assembly. The authors observed that fla mutants had properly assembled hearts with healthy myo- and endocardial cell layers but their cardiac tissue showed no contraction under stimulation. They also concluded that the cardiac electrical impulse was the same for both wild-type and fla embryos. Since no heart-related problems were found, this observation influenced the authors to look for a general muscular mechanism that has failed in these mutants. They therefore studied skeletal muscle function, and found that mutants, when touch-stimulated, generated "only a shiver response, which does not generate enough force for the fla embryo to execute a 'flight response '" (Just et al., 2011).
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Their key findings of defective myofibrillar organization was through assaying the muscle ultrastructure of fla mutants 48 hours post fertilization. The results are shown in Fig 1. above. These images show that sarcomerogenesis is absent in fast-twitch muscle tissues (Fig. 1D,F) and in cardiac tissue, but is very well defined in slow-twitch muscle tissue (Fig. 1H). Also, myosin bundles were never seen in fla mutant muscles, implying SMYD interferes with "early myosin assembly or stability" (Just et al.,

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