The tropical disease vector mosquito Anopheles gambiae possesses 11
rhodopsin genes. Three of these, GPROP1, GPROP3, and GPROP4, encode
rhodopsins with >99% sequence identity. We created
antisera against these
rhodopsins and used immunohistology to show that one or more of these
rhodopsins are expressed in the major R1-6 photoreceptor class of the adult A.gambiae eye. Under dark conditions,
rhodopsin accumulates within the light-sensitive rhabdomere of the photoreceptor. Light treatment, however, causes extensive movement of
rhodopsin to the cytoplasmic compartment.
Protein electrophoresis showed that the
rhodopsin is present in two different forms. The larger form is an immature species that is deglycosylated during the posttranslational maturation process to generate the smaller, mature form. The immature form is maintained at a constant level regardless of lighting conditions. These results indicate that
rhodopsin biosynthesis and movement into the rhabdomere occurs at a constant rate. In contrast, the mature form increases in abundance when animals are placed in dark conditions. Light-triggered internalization and protein degradation counteracts this
rhodopsin increase and keeps rhabdomeric
rhodopsin levels low in light conditions. The interplay of the constant maturation rate with light-triggered degradation causes
rhodopsin to accumulate within the rhabdomere only in dark conditions. Thus, Anopheles photoreceptors possess a mechanism for adjusting
light sensitivity through light-dependent control of
rhodopsin levels and cellular location.