We have data that support an intriguing cellular
model in Drosophila melanogaster for
a mechanism that facilitates differential adaptation to tropical and
cool-temperate climates. The model involves molecular variation in the hsr-omega gene that clines latitudinally
and influences rates of protein synthesis. Protein synthesis rates in turn
affect heat tolerance levels, especially the extent to which heat tolerance is enhanced
after a mild heat shock – other traits may also be affected. We are currently attempting
to elucidate details of the cellular mechanism using gene knockout mutants and
we are measuring several traits and protein synthesis rates in newly acquired
field strains collected over a broad latitudinal range. This will allow us to
assess modulation of protein synthesis as a mechanism for adaptation to different
climatic regions.
In this context the function of hsr-omega centres on variation among
strains in the level of functional units in the nuclear hsr-omega transcript (omega-n).
Lauren Carrington and Travis Johnson demonstrated that lines with high basal
levels of omega-n showed lower rates
of basal protein synthesis. Reviews of the cellular and molecular genetics of hsr-omega argue that a likely function
of the conserved sequence within the omega-n
repeats is to bind and ‘inactivate’ small nuclear proteins (and inactivate them
to a greater extent after heat induction of omega-n).These nuclear proteins are thought to be essential for splicing
intron-containing pre-mRNA into mature mRNA. If this proves to be correct it
provides a logical mechanism by which
hsr-omega variation influences rates of protein synthesis – high levels of omega-n lead to a lack of mature mRNA
from intron-containing housekeeping genes with the consequent slowing of
general protein synthesis. The shutdown of general protein synthesis is an
established component of the cellular heat shock response. In this model omega-n would not affect production of
the intronless heat shock proteins, such as hsp70, since their mature mRNAs
does not involve intron splicing. Hence, increased synthesis of heat shock
protein mRNAs after heat shock could proceed. Quantifying the levels of
pre-mRNA and mature mRNA of several key genes, both before and after an
appropriate heat shock will provide a test of this hypothesis/mechanism.