Similar processes occur during the original

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similar processes occur during the original development of muscle and neu- romuscular junctions. Reference: Sanes JR (2003) The basement membrane/basal lamina of skele- tal muscle. J. Biol. Chem. 278, 12601–12604. 19–55 The bacteria that secrete such enzyme are typically pathogenic bacteria that digest a protecting layer of basal lamina in order to invade their hosts and infect them. DATA HANDLING 19–56 Mice that are homozygous for knockout of the gene for either nidogen-1 or nidogen-2 presumably have no phenotype because the two forms of nido- gen can substitute for one another. Mice that are homozygous for the mutant form of laminin- g 1, which does not bind nidogen, have a much more severe phenotype than either of the individual nidogen gene knock- outs because they eliminate the ability of both nidogens to bind to laminin. As a result, these mice do not form proper basal lamina and die at birth with severe defects in kidney and lung. If this is the correct explanation for the genetic observations, then you would predict that mice that are homozy- gous for knockouts of both nidogen genes would have a very severe pheno- type, comparable to that of the laminin- g 1 mutant. Such mice have been made and they do have a severe phenotype. Reference: Sasaki T, Fassler R & Hohenester E (2004) Laminin: the crux of basement membrane assembly. J. Cell Biol. 164, 959–963. THE BASAL LAMINA A447
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19–57 The answer to this puzzle is not yet known. The basal lamina contains a complicated mixture of molecules including growth factors and growth inhibitors. Failure to cleave collagen (and other components) may lead to failure to release the signaling molecules that are essential for adipocyte development. Alternatively, it may be that the collagen cleavage products, themselves, provide differentiation signals to the preadipocytes. It could also be that these cells fail to correctly process signaling molecules on their own surface, or because they cannot penetrate the collagen tangle they do not come into contact with the signaling molecules on the surfaces of other cells. These hypotheses are difficult to test in intact animals, but isolated cells from mutant mice can be used to explore some of these possibilities. Reference: Chun T-H, Hotary KB, Sabeh F, Saltiel AR, Allen ED, Weiss SJ (2006) A pericellular collagenase directs the three-dimensional develop- ment of white adipose tissue. Cell 125, 577–591. INTEGRINS AND CELL–MATRIX ADHESION DEFINITIONS 19–58 Focal adhesion kinase (FAK) 19–59 Integrin 19–60 Anchorage dependence TRUE/FALSE 19–61 True. Tension—a mechanical signal—applied to an integrin can cause it to tighten its grip on intracellular and extracellular structures, including not only cytoskeletal and matrix components, but also molecular signaling complexes. Similarly, loss of tension can loosen its hold, so that molecular signaling complexes fall apart on either side of the membrane. Thus, the tension on the integrin can trigger or inhibit molecular signaling.
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  • Spring '04
  • EricLander
  • cell biology, Collagen, basal lamina, cell adhesion, J. Cell Biol.

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