Describe the Sev signaling pathway. Solution R7 cell plays an important role in study of RTK signaling processes in cell fate determination. Firstly, only two cells are involved, differentiated R8 cell as the signal sender and the presumptive R7 cell as the recipient. Secondly, depending on the presence or absence of the signal, the R7 precursor cell can only choose between the neuronal R7 and the non-neuronal cone cell fate, respectively. Thirdly, the presence of the R7 cell can be easily noticed in living animals. This allows extensive genetic screens for mutations that specifically interfere with the formation of the R7 cell and, therefore, might disrupt reception, transduction, or interpretation of the inductive signal in the R7 precursor cell. Two classes of mutations are anticipated. The first class is homozygous viable mutations like SEV which specifically affect R7 cell development. Few isolated mutations have met the criteria of specificity. The second class of mutations are more difficult to isolate. If the SEV cascade shares components with other RTKs like DER with multiple functions during development, animals homozygous for loss-of-function mutations in the corresponding genes would presumably die prior to R7 cell commitment. Simon used a temperature sensitive allele of sev (sevts) which provides barely sufficient activity to allow R7 cell development. The second approach involved expression of constitutively activated versions of SEV in all sev-expressing cells [20] and [21]. This resulted in transformation of cone cells into additional R7 cells resulting in a rough eye phenotype. The conclusion drawn from these experiments is that cone cell precursors are competent to respond to the inductive signal.R7 cell specification became sensitive to the gene dosage of rate-limiting components acting downstream of SEV. Hence, for a recessive lethal mutation, reducing the gene dose by half is sufficient to modify the sevts or the sevS11 phenotype, which can be scored in living animals. Large-scale screens conducted with both systems unravelled the first steps in the SEV signaling cascade..

1. Describe the Sev signaling pathway.
Solution
R7 cell plays an important role in study of RTK signaling processes in cell fate determination.
Firstly, only two cells are involved, differentiated R8 cell as the signal sender and the
presumptive R7 cell as the recipient. Secondly, depending on the presence or absence of the
signal, the R7 precursor cell can only choose between the neuronal R7 and the non-neuronal
cone cell fate, respectively. Thirdly, the presence of the R7 cell can be easily noticed in living
animals. This allows extensive genetic screens for mutations that specifically interfere with the
formation of the R7 cell and, therefore, might disrupt reception, transduction, or interpretation of
the inductive signal in the R7 precursor cell. Two classes of mutations are anticipated. The first
class is homozygous viable mutations like SEV which specifically affect R7 cell development.
Few isolated mutations have met the criteria of specificity. The second class of mutations are
more difficult to isolate. If the SEV cascade shares components with other RTKs like DER with
multiple functions during development, animals homozygous for loss-of-function mutations in
the corresponding genes would presumably die prior to R7 cell commitment. Simon used a
temperature sensitive allele of sev (sevts) which provides barely sufficient activity to allow R7
cell development. The second approach involved expression of constitutively activated versions
of SEV in all sev-expressing cells [20] and [21]. This resulted in transformation of cone cells
into additional R7 cells resulting in a rough eye phenotype. The conclusion drawn from these
experiments is that cone cell precursors are competent to respond to the inductive signal.R7 cell
specification became sensitive to the gene dosage of rate-limiting components acting
downstream of SEV. Hence, for a recessive lethal mutation, reducing the gene dose by half is
sufficient to modify the sevts or the sevS11 phenotype, which can be scored in living animals.
Large-scale screens conducted with both systems unravelled the first steps in the SEV signaling
cascade.