Paul
FlyBase has got itself confused (ie I am confused) about the
relationships to three 'genes; Arp, Psc and Su(z)2.
There are two ways of sorting this out.
1. MA goes to the library for two days.
2. MA asks a man or knows !
I enclose the information now in FlyBase on these genes. I would be
_very_ grateful if you could review it for us and tell
us what the real biology is !
Best
Michael
Subject: flybase
Michael,
Appended is a revised version of the flybase report you mailed
me. At the end I have added a note on the relationship between
Arp, Psc and Su(z)2.
Michael: I have made some corrections to the above, but I am not sure that all is correct as some
of it refers to work not done in my lab and I might have missed minor problems. In a number of
places Su(z)2 mutations are designated as PscSu(z)2x. Let me summerize some of my
conclusions. Psc is located proximal to Su(z)2. The genes are transcribed divergently and their 5'
ends are about 15 kb apart (this could be an overestimate as the 5' end of Psc was never well
mapped). The two genes encode related proteins. In(2L)Arp breaks the chromosome between
Psc and Su(z)2, but does not cause a loss of function in either. The juxtaposition of DNA from
49B upstream of Su(z)2 in In(2L)Arp results in a gain of function mutation in Su(z)2. This
causes the arista to tarsus transformation and the bristle abnormalities. The bristle loss
phenotypes of vg62 and vgD have a similar genetic basis. Indeed, we showed that
overexpression of a hs-Su(z)2 transgene at the appropriate developmental stage could mimic the
bristle loss phenotypes of these mutations (Sharp, Martin and Adler, Dev. Biol.  161:379-392 
(1994). The overexpression of Psc from a hs-Psc transgene will also cause similar bristle
phenotypes, but the overexpression of Psc is not involved in the gain of function phenotypes of
Arp, vg62 or vgD (indeed Psc is deleted in vg62 and vgD). The overexpression of Psc at
white prepupae results in substantial lethality and this may explain why no Psc overexpression
mutations have been isolated that are analogous to the Su(z)2 overexpression mutations.
Best wishes,
Paul