Monochromosome transfers to syrian hamster BHK cells via microcell fusion provide functional evidence for suppressor genes on human chromosome 9 both for anchorage independence and for tumorigenicity

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Abstract
We previously identified an anchorage independence‐suppressor gene, SAII, on rat chromosome (RNO) 5. RNO5 is homologous to human chromosomes (HSA) I and 9. In order to find the human homolog of the SAII gene, we transferred HSAI and HSA9 to an anchorage‐independent and tumorigenic Syrian hamster BHK 191‐5C cell line by microcell fusion. For HSA9, we used a t(X; 9)‐derivative chromosome to force the retention of this chromosome in hybrids by hypoxanthine‐aminopterin‐thymidine (HAT) selection. To study the possible effect of the X portion of the der(9)t(X; 9), we also transferred a normal X to 191‐5C cells. For HSAI, a neo‐tagged chromosome was introduced. Following the transfer of der(9)t(X; 9) to 191 ‐5C cells, the hybrid cells became anchorage dependent and nontumorigenic, and, upon the loss of this chromosome, the cells regained their tumorigenic and anchorage‐independent phenotypes. The transfer of HSAX or HSAI, on the other hand, affected neither of these phenotypes. These results provide functional proof of suppressor genes on HSA9 involving both anchorage independence and tumorigenicity. In addition, our data suggest the presence of another gene on HSA9 that causes a negative growth effect and whose phenotypic expression, contrary to the suppressor genes, is dosage dependent.