High impact information on sma-6

• Using genetic methods, we show that lon-1 lies downstream of the Sma/Mab signaling cascade and demonstrate that lon-1 mRNA levels are up-regulated in sma-6-null mutant animals [1].
• We then examined the ability of SMA-6 expression in different regions of the C. elegans body to rescue the sma-6 phenotype (small) and found that hypodermal expression of SMA-6 is necessary and sufficient for the growth and maintenance of body length [2].
• Using a SMA-6::GFP (green fluorescent protein) reporter gene, sma-6 was highly expressed in the hypodermis, unlike the type-II receptor DAF-4, which is reported to be ubiquitously expressed [2].
• Null mutations in sma-3 are at least as severe as null mutations in the ligand and type I receptor genes, dbl-1 and sma-6, indicating that the other Smads do not function in the absence of SMA-3 [3].
• To understand the mechanisms of body size control in C. elegans, we analysed sma-2, sma-4 and sma-6 small mutants in the DBL-1 pathway [4].

Biological context of sma-6

• The closest homologue is a Caenorhabditis elegans gene (Q09488) in cosmid C32D5.2 which shares 67% amino acid identity with Bp-trk-1 in the most conserved kinase domain (aa 259-482) [5].

Analytical, diagnostic and therapeutic context of sma-6

• In situ hybridization analysis revealed the spatial and temporal expression patterns of each clone and showed that at least four genes, including the gene for the type I receptor for DBL-1, sma-6, were transcriptionally regulated by the DBL-1 signal [6].

References