coordinated movements of gastrulation begin. This dramatic process transforms the simple hollow ball of cells into a multilayered structure with a central gut tube and bilateral symmetry.many of the cells on the outside of the embryo are moved inside it. Subsequent development depends on the interactions of the inner, outer, and middle layers of cells thus formed: the endoderm on the inside, consisting of the cells that have moved into the interior to form the primitive gut; the ectoderm on the outside, consisting of cells that have remained external; and the mesoderm between them, consisting of cells that detach from the epithelium to form a more loosely organized embryonic connective tissue. eventual pattern of muscles-in the limbs, for example-is determined by the routes that the migrant cells follow and the selection of sites that they colonize. The embryonic connective tissues form the framework through which the myoblasts travel and provide signals that guide their distribution. No matter which somite they come from, myoblasts that migrate into a forelimb bud will form the pattern of muscles appropriate to a forelimb, and those that migrate into a hindlimb bud will form the pattern appropriate to a hindlimb. Limb formation results from series of epithelial-mesenchymal inductions between the mesenchymal cells of the lateral plate mesoderm and the overlying ectodermal cells. Cells from the lateral plate mesoderm and the myotome migrate to the limb field and proliferate to create the limb bud. The lateral plate cells produce the cartilaginous and skeletal portions of the limb while the myotome cells produce the muscle components. The lateral plate mesodermal cells secrete a fibroblast growth factor (FGF7 andFGF10, presumably) to induce the overlying ectoderm to form an important organizing structure called the apical ectodermal ridge(AER).The AER reciprocatively secretes FGF8 and FGF4 which maintains the FGF10 signal and induces proliferation in the mesoderm.[citation needed] The position of FGF10 expression is regulated by Wnt8c in the hindlimb and Wnt2b in the forelimb. The forelimb and the hindlimb are specified by their position along the anterior/posterior axis and possibly by two T-box containing transcription factors: Tbx5 and Tbx4, respectively. DKK1 activation in osteoblasts is the underlying cause of glucocorticoid- and estrogen deficiency–mediated osteoporosis, and at least partially underlies the teratogenic effects of thalidomide on limb development. both thalidomide-induced PCD and limb deformities could be partially inhibited by blocking Dkk1 or activating Wnt signaling downstream of the ligand-receptor interaction Solution coordinated movements of gastrulation begin. This dramatic process transforms the simple hollow ball of cells into a multilayered structure with a central gut tube and bilateral symmetry.many of the cells on the outside of the embryo are moved inside it. Subsequent development depends on the interactions .

1. coordinated movements of gastrulation begin. This dramatic process transforms the simple
hollow ball of cells into a multilayered structure with a central gut tube and bilateral
symmetry.many of the cells on the outside of the embryo are moved inside it. Subsequent
development depends on the interactions of the inner, outer, and middle layers of cells thus
formed: the endoderm on the inside, consisting of the cells that have moved into the interior to
form the primitive gut; the ectoderm on the outside, consisting of cells that have remained
external; and the mesoderm between them, consisting of cells that detach from the epithelium to
form a more loosely organized embryonic connective tissue.
eventual pattern of muscles-in the limbs, for example-is determined by the routes that the
migrant cells follow and the selection of sites that they colonize. The embryonic connective
tissues form the framework through which the myoblasts travel and provide signals that guide
their distribution. No matter which somite they come from, myoblasts that migrate into a
forelimb bud will form the pattern of muscles appropriate to a forelimb, and those that migrate
into a hindlimb bud will form the pattern appropriate to a hindlimb.
Limb formation results from series of epithelial-mesenchymal inductions between the
mesenchymal cells of the lateral plate mesoderm and the overlying ectodermal cells. Cells from
the lateral plate mesoderm and the myotome migrate to the limb field and proliferate to create the
limb bud. The lateral plate cells produce the cartilaginous and skeletal portions of the limb while
the myotome cells produce the muscle components. The lateral plate mesodermal cells secrete a
fibroblast growth factor (FGF7 andFGF10, presumably) to induce the overlying ectoderm to
form an important organizing structure called the apical ectodermal ridge(AER).The AER
reciprocatively secretes FGF8 and FGF4 which maintains the FGF10 signal and induces
proliferation in the mesoderm.[citation needed] The position of FGF10 expression is regulated
by Wnt8c in the hindlimb and Wnt2b in the forelimb. The forelimb and the hindlimb are
specified by their position along the anterior/posterior axis and possibly by two T-box containing
transcription factors: Tbx5 and Tbx4, respectively.
DKK1 activation in osteoblasts is the underlying cause of glucocorticoid- and estrogen
deficiency–mediated osteoporosis, and at least partially underlies the teratogenic effects of
thalidomide on limb development.
both thalidomide-induced PCD and limb deformities could be partially inhibited by blocking
Dkk1 or activating Wnt signaling downstream of the ligand-receptor interaction
Solution
coordinated movements of gastrulation begin. This dramatic process transforms the simple

2. hollow ball of cells into a multilayered structure with a central gut tube and bilateral
symmetry.many of the cells on the outside of the embryo are moved inside it. Subsequent
development depends on the interactions of the inner, outer, and middle layers of cells thus
formed: the endoderm on the inside, consisting of the cells that have moved into the interior to
form the primitive gut; the ectoderm on the outside, consisting of cells that have remained
external; and the mesoderm between them, consisting of cells that detach from the epithelium to
form a more loosely organized embryonic connective tissue.
eventual pattern of muscles-in the limbs, for example-is determined by the routes that the
migrant cells follow and the selection of sites that they colonize. The embryonic connective
tissues form the framework through which the myoblasts travel and provide signals that guide
their distribution. No matter which somite they come from, myoblasts that migrate into a
forelimb bud will form the pattern of muscles appropriate to a forelimb, and those that migrate
into a hindlimb bud will form the pattern appropriate to a hindlimb.
Limb formation results from series of epithelial-mesenchymal inductions between the
mesenchymal cells of the lateral plate mesoderm and the overlying ectodermal cells. Cells from
the lateral plate mesoderm and the myotome migrate to the limb field and proliferate to create the
limb bud. The lateral plate cells produce the cartilaginous and skeletal portions of the limb while
the myotome cells produce the muscle components. The lateral plate mesodermal cells secrete a
fibroblast growth factor (FGF7 andFGF10, presumably) to induce the overlying ectoderm to
form an important organizing structure called the apical ectodermal ridge(AER).The AER
reciprocatively secretes FGF8 and FGF4 which maintains the FGF10 signal and induces
proliferation in the mesoderm.[citation needed] The position of FGF10 expression is regulated
by Wnt8c in the hindlimb and Wnt2b in the forelimb. The forelimb and the hindlimb are
specified by their position along the anterior/posterior axis and possibly by two T-box containing
transcription factors: Tbx5 and Tbx4, respectively.
DKK1 activation in osteoblasts is the underlying cause of glucocorticoid- and estrogen
deficiency–mediated osteoporosis, and at least partially underlies the teratogenic effects of
thalidomide on limb development.
both thalidomide-induced PCD and limb deformities could be partially inhibited by blocking
Dkk1 or activating Wnt signaling downstream of the ligand-receptor interaction