Worm Breeder's Gazette 15(4): 34 (October 1, 1998)
We are interested in understanding TGFb signaling pathway. Work in several laboratories has led to a model in which Smad proteins are activated by phosphorylation by TGFb receptors allowing them to translocate to the nucleus and act as transcriptional activators. There is a continued interest in identifying new components of this pathway. Sma-9 is a putative member of this pathway. Complementation tests have shown that there are four alleles of sma-9 -- wk55, wk62, wk71, and wk82. Another sma-9 allele, wk121, was kindly given to us by S. Cohen and R. Padgett. Genetic screen described below has yielded us with one more allele of sma-9, which is named qc1.
Sma-9 expresses the classical phenotype expressed by other sma genes. It affects body size and male tail ray patterning. Sma-9 mutant animals are small in size. We have examined males for the four sma-9 alleles (wk55, wk62, wk71, and wk82) for ray patterning defects (see Table 1 for that).
To increase the frequency of males, we made him-5(e1490);sma-9 doubles for all four of sma-9 alleles. In fact, we had initially made doubles with him-8(e1467). However, Scott Emmons had pointed out to us at the Worm Meeting that this him-8 strain has males that are not wild type. They have ray patterning defects of their own. We checked by examining about seven male tail sides using the Nomaraski Microscopy. They all had fusions of rays 8 and 9. And strangely enough, our sma-9 males also exhibit fusions of rays 8 and 9. We also examined him-5 males. Even they exhibited fusions of rays 8 and 9, however, at a lower frequency. However, this fusion of 8 and 9 is different from the one exhibited by sma-9 males. In him-5 and him-8 males, when rays 8 and 9 are fused, the fused ray resembles ray 9, whereas in the sma-9 fusion of rays 8 and 9, the fused ray resembles ray 8.
Besides male tail characterization, we are also interested in generating new mutations in sma-9. So far, we have done six EMS mutagenesis experiments. Mutagenized N2 males were crossed with sma-9unc-7 hermaphrodites. And in the F1 generation, we scored non Unc hermaphrodites. We have obtained one new sma-9 allele, qc1 from 5700 chromosomes scored. The complementation test has shown that it is in fact, a new sma-9 allele.