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Table 1 Postemergence maturation defects associated with disabling RK function in different cell types

From: The tanning hormone, bursicon, does not act directly on the epidermis to tan the Drosophila exoskeleton

Tissue targeted1

Driver2

Pigmentation defects3

Sclerotization defects4

Wing expansion defects5

Cuticle appearance6

RK cells

rk-GAL4

+++ 7

+++

+++

+++

Epidermis

TH-GAL4

+++

Tendon cells

sr-GAL4

Hemocytes

hem-GAL4

Muscles

C59-GAL4

Oenocytes

desat(RE)-GAL4

Neurons

elav-GAL4

+++

+++

+++

+++

nsyb-GAL4

+++

ND

+++

+++

Peptidergic neurons

amon-GAL4

+++

ND

+++

++

dimm-gal4

++

ND

ILP7 neurons

ilp7-GAl4

++

ND

  1. 1Tissues in which RK function was disabled by driving tBur
  2. 2GAL4 driver used to drive UAS-tBur in desired tissues
  3. 3–6 Defects observed in pigmentation 3; sclerotization 4 (assessed measuring soluble protein present in cuticle); in wing expansion 5 and in cuticle appearance 6 (incomplete maturation causes cuticle to have a surface that is matte in appearance)
  4. 7 Defects were classified qualitatively as severe (+++; similar to those of rk mutant animals) to normal (−). ND not determined