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Fig. 4. Premigratory to migratory neural crest: sequential activation of migratory
potential. The array of genes expressed 24 hours after neural crest induction,
coupled with temporal analysis of expression patterns throughout neural crest
development, make it possible to assemble a hypothesis for acquisition of
migratory capacity. Following initial induction, cells in the neural folds
begin the process of becoming neural crest cells (blue rectangles) by
expressing intermediate filaments, proliferation factors, receptors and
secreted signals, and increased transcriptional machinery (including known
transcription factors such as slug). This is followed by the acquisition of
migratory potential (yellow asterisks) with expression of components of the
actin cytoskeleton, rho targets, extracellular matrix, and translational
machinery. The signal to migrate mobilizes this migratory potential (yellow
cell) through the activation of rho targets
(Liu and Jessell, 1998 ) as a
consequence of signaling through the BMP pathway
(Sela-Donenfeld and Kalchiem,
1999) or asymmetric cell division
(Erickson and Reedy, 1998).
This results in the delamination of some cells from the neural folds. Cells
that remain in the neural folds never access their migratory potential and
become dorsal neural tube. Green: cytoskeleton; orange: proliferation; red:
cell surface/signaling; purple: gene expression.
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5; (D) hexokinase 1, isoform HKI; (E)
KIF4a/chromokinesin; (F) Nopp140; (G) GCN20/ATP-binding
cassette transporter F2; (H) tyrosine kinase receptor KLG; (I)
MSE55; (J) dyskerin; (K) thimet oligopeptidase; (L)
E12; (M) UV DNA damage binding protein 1; (N) cationic
amino acid transporter 3; (O) D52-like 2; (P) human
KIAA0147. (Q-X) Transverse sections, dorsal up. (Q) cathepsin D;
(R) alanyl tRNA synthetase; (S) UV DNA damage binding
protein; (T) CFR-associated protein; (U) paranemin; (V)
laminin 