Worm Breeder's Gazette 15(5): 45 (February 1, 1999)

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

Mapping sma-9

Gayatri Mirani, Cathy Savage-Dunn

Department of Biology, Queens College, CUNY, Flushing, NY 11367

We are interested in understanding TGFb signaling pathway. One of the newest members of this pathway that has been identified is sma-9. In the last article we published in the Worm Gazette, we wrote about the male tail ray patterning exhibited by sma-9 mutant males. Besides characterizing male tail ray patterning, we are also interested in figuring out where sma-9 maps and how sma-9 may function in TGFb signaling pathway.

When we crossed sma-9 hermaphrodites with wild type males, we got small males in the next generation. That proved to us that sma-9 mapped to the X chromosome and it had to be recessive because we also got wild type hermaphrodites. We decided to use two-factor mapping to figure out where exactly sma-9 mapped on the X chromosome. We made three sma-9unc doubles using three unc genes (unc-2, unc-7, and unc-9) and crossed them with wild type males. In the F2 generation, we looked for rare recombinants (in this case, small nonuncs and unc nonsmalls). Using the data we obtained, we found the map distance (p; Brenner, 1974) of sma-9 relative to each unc gene and obtained the following results:

 

Table 1. Map position of sma-9 relative to 3 unc genes as obtained from the two-factor mapping

 

Gene

 

Map Position

 

Wild Type

 

Small Nonunc

 

Unc Nonsmall

 

Small Unc

 

Total

 

p

 

unc-2

 

-13.5

 

534

 

123

 

125

 

218

 

1000

 

29.0

 

unc-7

 

+20.5

 

813

 

86

 

101

 

259

 

1259

 

16.2

 

unc-9

 

+11.5

 

809

 

27

 

18

 

184

 

1038

 

4.4

 

These data suggest that sma-9 maps to the interval between +4 and +15. To figure out where exactly sma-9 mapped in that interval, we decided to use duplications and deficiencies. We chose duplications and deficiencies that covered either the rightmost or the leftmost of this interval. Two duplications we used were-- yDp9 (left) and mnDp1(right). Two deficiencies we used were-- nDf19 (left) and mnDf1(right). The crosses using these duplications and deficiencies proved that nDf19 and yDp9 include sma-9 but mnDf1 and mnDp1 do not. This smaller interval extends from +4 and +7. Even though we have narrowed the interval to which sma-9 maps considerably, it is not small enough to allow us to clone this gene. We are using STS (Sequence-Tagged Sites) for a finer mapping.

Since sma-5 maps to this interval, we thought sma-5 might turn out to be just another mutation of sma-9. However, complementation tests using three sma-9 alleles (wk62, wk71, and wk82) showed that sma-9 and sma-5 complement. So sma-9 and sma-5 are two different genes. Yet it is possible that sma-5 may be a different kind of mutation of the sma-9 gene.