Subject: Re: Help FlyBase please
>Jim
>
>Thanks. Yes I had a reply from Lisa, which was not very clear.
>
>My interpretation is that there are four genes on this sequence - as judged
>by coding content:
>
>27..963 Nacα
>1138..2911 Dgkε
>3189..3519 Ucr9
><4457..>4720 tafazzins
>
>There is also the P-element associated with oxen1 at 3147
>
>The confusing thing is that the record says:
>
> mRNA 27..963
> /gene='oxen'
> /product='alpha NAC'
> gene 27..963
> /gene='oxen'
>
>which I take to mean that the product of oxen is Nacα and I assume
>you have some other evidence for this, given the fact that the ox1 P
>insertion is between the 5' ends of Dgkε and Ucr9.
>
>Correct ?
>
>Michael
Michael:
	OK, let me see if I can explain the sequence of events. The first
entry to Genbank several years ago reported the aNAC sequence. It was
identified by rescue of the ox1 P element and probing a cDNA library with
the surrounding sequences. The level of aNAC RNA is reduced in the ox1
mutation, but not in the revertant. For that reason, oxen was included in
the gene entry.
	Further work over the years has revealed a morass of closely packed
genes in the region. These data suggest that the primary lesion of oxen is
not an effect on aNAC, although given the dense and overlapping
organization of this region, it is possible that the lesion affects several
genes. The updated entry to Genbank included a request to remove the gene
entry as being oxen, but this did not occur. We have sent another
communication making this request again.
	The ox1 mutation affects the RNA levels of aNAC, Dgk and Qcr9.
Transformants of aNAC do not rescue the mutant phenotype of ox1.
Transformants of Dgk do not rescue the mutant phenotype of ox1.
Transformants of Qcr9 are in progress, so we don't know the answer yet.
(Note that the orthologous gene in yeast that you abbreviated as Ucr9 is
referred to as QCR9.)
	The bottom line is that we do not know definitively which of these
genes corresponds to the ox1 mutation. It is even possible that the ox1
mutation affects several genes in this region and that the mutant phenotype
is a combination effect. I believe that the best course of action is to
hold in abeyance the assignment of a gene to the ox1 mutation. Can
Flybase deal with that ambiguity for the time being?
	Let me know if you need further information.
					Regards,
					Jim
James A. Birchler
Professor of Biological Sciences
University of Missouri
117 Tucker Hall
Columbia, MO 65211