Biomedical Engineering Reference
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Figure 2 . Ventral ectodermal patterning. In the graphs, the y -axis is the Egfr activity and the x -
axis the distance away from the midline. All cells are initially uniform. Patterning is initiated
by secretion of Spitz from the midline cells. This creates a graded activation of EGFR and
induction of the low-threshold ventrolateral fate (dotted) in nearby ectodermal cells. In time,
the signaling activity increases such that the cells nearest to the midline (striped) reach the high
threshold of the ventral-most fate and start secreting Argos. Inhibition by Argos modifies the
gradient of activity, restricting the domain of each ventral fate. This pattern persists for at least
3 more hours. (Note: The timeline is approximated from various published data.)
Subsequently, the cells nearest to the midline, hence the ones exposed to the
highest level of Spitz, start secreting Argos. This establishes a negative feedback
that is thought to refine the gradient of Spitz-induced EGFR activity and regu-
late the relative number of cells adopting each of the ventral fates. As a result of
the interplay between Spitz and Argos, five rows of cells flanking the midline
are patterned. The two rows nearest to the midline receive a high level of EGFR
activation and adopt the ventral-most fate. The next three rows of cells receive a
moderate level of EGFR activation and adopt the ventrolateral fates. In sum-
mary, the initial gradient of EGFR activity induced by a localized secretion of an
activator (Spitz) is refined by a secreted inhibitor (Argos), creating two distinct
fates.
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