Muscle biology - Elisabeth Ehler

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Dear Jen and Midori, I can't add that much. Elisabeth has done sterling work. I would add however the 'transitional junction' (TJ) that lies at the same point and replaces the Z-disc of the terminal half sarcomere of cardiac myocytes. The TJ maintains connectivity and tension with the actin filaments that enter the adherens junction at the intercalated disc. Ref Bennett et al MBC (2006) v17 2091-2100. In this paper we also describe the ID membrane 'steps' and 'risers'. There is a lot more to come out the the structures in this region of the ID, but for the moment we can leave it at that. I could also add the 'cardiac cytoskeleton' opr to be more accurate perhaps the 'cardiac membrane skeleton' as distinct from the known actin, tubulin and intermediate filament systems. It is not that clear that it is exclusively involved with membranes however!! The main components are spectrin, protein 4.1 and ankyrin. We reviewed it in Baines and Pinder (2005) Frontiers in Bioscience vol 10 3020-3033 where we called it the 'spectrin-associated cytoskeleton' I hope these comments are clear - please come back to me for more information if wanted. Best wishes, Jeni


Dear Jen, dear Midori, here is my "homework!

oscillatory contraction: I sent an email to Prof Belinda Bullard at the University of York, who is an expert on this subject and also on the fly sarcomere.


I think that Jeni Fordhamn & I agree that the specialised membranes of muscle are still underrepresented at present: This would include areas like

Triads: Muscle membrane invaginations (= T-tubules) in close association with the sarcoplasmic reticulum (SR) that help to transform the action potential to a stimulus that triggers calcium release by the SR; in cardiac muscle situated close to the Z-disc; in skeletal muscle at the I/A-band junction. (Clara Franzini-Armstrong has done the ground-breaking work on those)

Intercalated disc: Specialised type of cell-cell junction in cardiac muscle, which mediates mechanical and electrochemical integration between the individual cardiomyocytes. Consist of three different kinds of substructures: adherens junctions (anchorage sites of actin filaments or in the case of muscle cells, myofibrils to the plasma membrane), desmosomes (anchorage sites of intermediate filaments to the plasma membrane) and gap junctions (ion channels that consist of connexin-43).

Myotendinous junction: Terminal anchorage site of skeletal muscle cells to tendons; specialised type of contact between the cell and the extracellular matrix in skeletal muscle.

Costameres: Lateral contacts between the cells and the extracellular matrix in cardiac and skeletal muscle cells. Have a rib-like appearance on the surface of the cells (hence costameres) and provide a cytoskeletal link from the Z-disks to the plasma membrane. PMID: 6405378 (IDA)

Dystrophin glycoprotein complex: Junction between the cytoskeleton (dystrophin) and the extracellular matrix (laminin) that involves members of the dystroglycan and sarcoglycan family as transmembrane components.

Caveolae: membrane invaginations that are characterised by the presence of the protein caveolin and richness in cholesterol.


EE version of some other definitions that I noted down during the final discussion:

Hypertrophy: Increase in cell mass due to growth of the individual cell; in case of striated muscle cells this happens due to the additional synthesis of sarcomeric proteins and assembly of myofibrils. Physiological hypertrophy is the normal process during development (stops e.g. in cardiac muscle after adolescence) or caused by additional demand (cardiac and skeletal muscle growth in athletes; cardiac and smooth muscle (uterus) hypertrophy in pregnant women); pathological hypertrophy is the process, when the growth (induced by a pathological stimulus such as hypertension; mutation in a muscle protein) runs out of control and the additional tissue mass can no longer be supplied properly by the vasculature, this leads to hypertrophic cardiomyopathy.

Hyperplasia: Increase in cell mass due to cell proliferation; in cardiac muscle almost exclusively seen during embryonic development and no longer observed after birth.

Atrophy: Decrease in cell mass due to shrinking of the individual cell caused by protein degradation.


Titin: synonym should include "connectin", the way it was originally called (PMID: 1002676)



M-band components:

Myomesin: its gene is MYOM-1; alternative names are skelemin (previous name of a longer myomesin splice variant) Swissprot mouse: MYOM1_MOUSE, Q62234; human: Myom1-human, P52179) PMID: 6537951 (IDA)

M-protein: its gene name is confusingly MYOM-2 and a few morons also call it myomesin-2 (Swissprot mouse: O55124; human: myom2-human, P54296) PMID: 4209974 (IDA)

Muscle creatine kinase: M-CK (Swissprot mouse: KCRM_MOUSE, P07310) PMID: 4197625

myosin heavy chain (C-terminus only!)

titin (C-terminus only)

Obscurin: (Swissprot human OBSCN_HUMAN, Q5VST9) PMID: 11448995 (IDA)

DRAL/FHL-2: (Swissprot human: 13229, Q14192, FHL2_HUMAN, Q13644, Q9P294) PMID: 12432079 (IDA)

Enolase PMID: 9931306 (IDA)