TABLE Q19-1 Phenotypes of mice with genetic defects in components of the basal lamina (Problem 19-8). Protein Genetic defect Phenotype Nidogen-1 Gene knockout (-/-) None Nidogen-2 Gene knockout (-/-) None Nidogen binding-site deletion (+/-) Laminin y-1 None Laminin y-1 Nidogen binding-site deletion (-/-) Dead at birth +/- stands for heterozygous, -/- stands for homozygous.
Structure and Composition of Cell Membrane
Despite differences in structure and function, all living cells in multicellular organisms are surrounded by a cell membrane. Just like the outer layer of the skin separates the body from its environment similarly, the cell membrane, also known as 'plasma membrane,' separates the inner content from its exterior environment.
Cell Membrane
The cell membrane is known by different names like plasma membrane or cytoplasmic membrane, or biological membrane. The term "cell membrane" was first introduced by C. Nageli and C. Cramer in the year 1855. Later on, in 1931, the term "plasmalemma" for cell membrane was given by J. Plowe. The cell membrane separates the cell's internal environment from the extracellular space. This separation allows the protection of cells from their environment.
Prokaryotes vs Eukaryotes
The cell is defined as the basic structural and functional unit of life. The cell membrane bounds it. It is capable of independent existence.
It is not an easy matter to assign particular func-
tions to specific components of the basal lamina, since
the overall structure is a complicated composite material
with both mechanical and signaling properties. Nidogen,
for example, cross-links two central components of the
basal lamina by binding to the laminin γ-1 chain and to
type IV collagen. Given such a key role, it was surprising
that mice with a homozygous knockout of the gene for
nidogen-1 were entirely healthy, with no abnormal phe-
notype. Similarly, mice homozygous for a knockout of the
gene for nidogen-2 also appeared completely normal. By
contrast, mice that were homozygous for a defined muta-
tion in the gene for laminin γ-1, which eliminated just the
binding site for nidogen, died at birth with severe defects
in lung and kidney formation. The mutant portion of the
laminin γ-1 chain is thought to have no other function
than to bind nidogen, and does not affect laminin struc-
ture or its ability to assemble into the basal lamina. How
would you explain these genetic observations, which are
summarized in Table Q19–1? What would you predict
would be the
for knockouts of both nidogen genes?
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