Subject: Sb
Correction to FLYBASE information of Sb.
Dear Flybase:
After happily cruising Flybase for info on regions of interest to my
current post-doctoral research, I have finally gotten around to
looking up the subject of my PhD work, Sb-sbd.  Much to my
chagrin, I have discovered that the person in my old lab who was
supposed to send in the new information to the Redbook
consortium in 1992 never did.  You have some information from
our PNAS paper (FBrf0059263 == Appel et al., 1993, Proc. natn.
Acad. Sci. USA. 90(11): 4937--4941), but there is more information
in my thesis (Appel, L.F. (1992) Ph. D. thesis, University of
California, Berkeley).
First off, the cytological location Flybase uses for Sb is wrong.
You & Redbook say
'Cytological map position :
   Placed in 89B4-5, probably in 89B4, by Lewis (1951).
   This probably corresponds to 89B9-10 on Bridges's
   revised map.'
This is correct, but then Cytosearch uses the old version (89B4-5).
It should use the new version (89B9-10).
Under 'Other information' you say
'Authors consider that Sb and sbd are represented by the same transcript,
      although no discussion of this point is explicitly included.'
The figure and discussion in the PNAS paper show that both sbd
and Sb alleles are associated with DNA lesions within the same
transcription unit.  The issue is addressed explicitly in the thesis.
The lethality of Sb1 is probably not due to Sb, but to a second
mutation on the same chromosome called l(3)89Aa, identified by
Nelson and Szauter. (FBrf0057262  Nelson, C. R. and  Szauter, P.
(1992). Cytogenetic analysis of chromosome region 89A of
Drosophila melanogaster,. Mol. and Gen. Genetics  235, 11-21.)
I have several notes  for you about sbd26.
First, the cytology of Df(3R)sbd26 is also incorrect, this time due to
a typo.
Flybase says:
'Aberration symbol        : Df(3R)sbd26
Last updated             : 21 Feb 95
Full name                : Deficiency (3R) stubbloid
FlyBase aberration id    : FBab0002924
Breakpoints              : 87C7-87D1;89B9-89B10'
Later in the reference there are the correct breakpoints:
   'Breakpoints              : 89B9-89B10;89C7-89D1'
It looks like 89 turned into 87 at some point during transcription.
89 is correct.
In addition, the sbd and the deficiency are probably independent.
The proximal breakpoint of the deficiency mapped at least 112 kb
away from the nearest part of the transcript.
More importantly, most stocks advertizing themselves as
Df(3R)sbd26 are actually Df(3R)sbd45.  (26 deletes from 89B9-10
distal, 45 deletes from 89B9-10 proximal.) This was true of stocks
from every stock center I tried, including Indiana and Umea (and
the stock we had in the Fristrom lab and had published based on
previously).  Luckily, Szauter still had the real thing.  Outcrossing
to ss- is diagnostic: Df(3R)sbd45 complements, Df(3R)sbd26 does
not.  If Indiana's stock dates from prior to 1992, it is probably
wrong, and should be replaced with the Fristrom or Szauter lab's
correct version.
For sbd104, Flybase lists only
'Parent aberration        : Tp(3;3)sbd104
Aberration symbol        : Dp(3;3)sbd104
Last updated             : 21 Feb 95
FlyBase aberration id    : FBab0010059'
Flybase should list the deficiency as well as the transposition, so it
will come up under ' --- Deleted segments'
For the rest of the alleles, I append here a table and paragraph
from my thesis. It includes all Sb and sbd alleles I am aware of.  I
made serious efforts to get hold of SbW and the Spillman-Faller
sbds other than 26 and 45 -- I am convinced that they no longer
exist and Flybase should not get anyone's hopes up by listing them
without asterisks.
Table 3.1	Alleles of the Stubble-stubbloid locus.
	Allele	(alternate NotesOrigin
		  name)
Stubble  alleles
	 Sb1		>	Spontaneous; Bridges, 1923.
	 Sb63b		>	Spontaneous; Merriam, 1963.
	 Sb70		>	Spontaneous.
	 SbSpi	(Spike)		X-ray; Moore, 1931.
	 SbV			X-ray, T(2;3);  Lewis, 1948.
				Variegates to +, progenitor Sb1.
    	 SbW 		*	Found in the wild, Crow; no longer exists.
stubbloid  alleles
	 sbd1	(Sbr)		Spontaneous; Sturtevant, 1926.
	 sbd2			Spontaneous; Harnley.
	 sbd2Sb1			Recombination;  Lewis, 1952.
	 sbdlethal(sbdl)	>	X-ray; Lewis. associated with  T(2;3) Me; TM1.
	 sbd26		>:	X-ray, Df; Spillman-Faller, 1978,
	 sbd45		>	X-ray, Df; Spillman-Faller, 1978.
   	 sbd##		*	Other sbd alleles generated by Spillman-Faller,
				 all of which had had two-digit designations,
				  no longer exist.
	 sbd104		>	X-ray, Tp( 3:3 ); Lewis, 1947; also Df by
					recombination.
	 sbd105		>	X-ray, Df; Lewis, 1948.
	 sbd106		>	X-ray, T(2;3); Lewis.
	 sbd201	(dtd 20-1)	EMS; Beaton & Fristrom, 1986.
 	 sbd203	(sbd71)	%	Bevatron (Niobium, 500 rads); Hammonds, 1989.
 	 sbd204	(sbd89)	%	Bevatron (Niobium, 500 rads); Hammonds, 1989.
 	 sbd206	(sbd28)	@	EMS; Hecht, 1989.
  	 sbd207	(sbdG73)$	Gamma irradiation; Gelbart, 1973.
	 sbd208	(sbdlG)	$	Spontaneous, McCarron.
   	 sbd210	(sbd91h)=	Found in wild, Auburn Calif., M. Green, 1991.
	 sbdGT11		>~	Gamma irrad., T(2;3); Ashburner. (Gubb et al.)
  	 sbdPNR11  	  ~	EMS; Heitzler and Simpson, 1991.
	 sbdVX1  	>~	X-ray; Heitzler and Simpson, 1991.
  	 sbdVE2  	  ~	EMS; Heitzler and Simpson, 1991.
  	 sbdVE3 		  ~	EMS; Heitzler and Simpson, 1991.
Stubble  Revertants (all are sbd)	
	 sbd202r	(Sb63bR1, Rev1)	>&	DEB; Surh, Beaton and Fristrom, 1987.
	 sbd205r	(sbdC34)	>&	P-element (D2-3/Birm-2); Appel and
Bayer, 1989.
  	 sbd209r	(sbdF57)	$	Spontaneous revertant of Sb1; McCarron.
   	 TM3 Sb1R+SE1 Ser 	  ~	EMS; Heitzler and Simpson, 1991.
  	 TM3 Sb1R+SE2 Ser 	  ~	EMS; Heitzler and Simpson, 1991.
	 TM3 Sb1R+SX3 Ser 	>~	X-ray; Heitzler and Simpson, 1991.
  	 TM3 pnrD4 Sb1R+SX4 Ser   ~	X-ray; Heitzler and Simpson, 1991.	
Other strains
  	 TM3 pnrD4 Sb1 Ser	  ~	Progenitor of  pnrD4R+3 and Sb1R+SX3.
  	 TM3 pnrD4R+3 Sb Ser 	  ~	X-ray; small Df just proximal to, but
					not altering, Sb1.  Heitzler and 	
					Simpson, 1991.
	bxd100		>	X-ray, Tp(3;3); Lewis; also available
				as Df by recombination; sbd+; just
				distal to Sb-sbd.
Notes.
> 	indicates DNA polymorphisms found in walk.
\* 	indicates strains that have been lost over time.
 :	most strains called Df(3R)sbd26 in US and Europe are actually
	Df(3R)sbd45. 	Cross 	to ss- is diagnostic for real
	sbd26 deficiency, which may be independent of sbd26
	mutation, see text.
Source of mutants not found in Lindley and Zimm (1992):
% 	Fristrom laboratory, UC Berkeley; progenitor red e.
@ 	Anderson laboratory, UC Berkeley; progenitor rucuca.
$ 	Chovnick laboratory, University of Connecticut.
~ 	Simpson laboratory, Faculte de Medecine, Strasbourg, France;
	   progenitors st e  or TM3 Sb Ser.
&	Fristrom laboratory, UC Berkeley; progenitor Sb63b.
=	Mel Green, UC Davis.
	Of the Sb alleles, Sb1, SbV, and SbSpi are much less severe in
phenotype, both in bristle length and frequency and severity of
malformation of appendages, than Sb63b and Sb70.  sbd1, sbd2 and
sbdG73 have much milder phenotypes than other sbd alleles.  They
are viable and not malformed as homozygotes.  All other sbd
alleles, including the Sb revertants, have shorter bristles than
these three, and are malformed (though not every individual) as
homozygotes or transheterozygotes. There are no viable alleles
than can safely be called nulls.  The two deficiencies which
remove the entire gene, Df(3R)sbd45 and Df(3R)sbd105 are lethal
both as homozygotes and as a transheterozygote.  The
Df(3R)sbd26/Df(3R)sbd105 transheterozygote gives viable
malformed escapers, but as discussed earlier, the sbd26 mutation
may be independent of the deficiency.  The inversion that breaks
the gene before the start of translation, In(3R)sbdVX1, has a more
severe phenotype as a homozygote than over a deficiency,
suggesting that it is not a true null.  Both that inversion and the
translocation T(2;3)sbdGT11 could have influences from promoters
or enhancers in the foreign upstream DNA.  The sbd205r insertion
is also before the start of translation, but its transcript has not been
sufficiently characterized to call it a null.  All of the other mutants
mapped could make truncated proteins.
I hope this is of use.  Let me know if you have questions, or want
more information. You may reference this either to my thesis or
as personal communication.
Sincerely,
Laurel F. Appel
Dept. of Biology
Shanklin and Hall-Atwater Laboratories
Wesleyan University
Middletown, CT  06459-0170