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INTRODUCTION <br />The problem of hybridization between razorback suckers <br />(Xyrauchen texanus) and flannelmounth suckers (Catostomus <br />latipinnis) can be addressed using allozyme characters if <br />suitable diagnostic "marker loci" are identified. These loci, <br />that express different alleles in each of these species, would <br />be expected to be heterozygous for the two parental alleles at <br />all marker loci in the F1 generation. Reassortment in the F2 and <br />subsequent generations, and backcrosses, would yield lesser <br />degrees of heterozygosity. However, remnant alleles from the <br />original hybridization event serve to indicate that such genetic <br />contamination had occurred. <br />Buth et al. (1987) found a surprisingly high level of <br />genetic similarity between razorback and flannelmouth suckers <br />(Neils 1978 genetic identity of 0.80) that would not have been <br />expected of catostomid species that are not particularly closely <br />related (following Smith 1992). Nevertheless, four marker loci <br />were identified: creatine kinase (Ck-A), glucose-6-phosphate <br />isomerase (Gpi-A2), isocitrate dehydrogenase (mIcdh-A), and <br />superoxide dismutase (sSod-A2). No F1 hybrids were identified <br />and the introgression at the four marker loci was unequal: low <br />levels for Ck-A and mIcdh-A, no introgression at Gpi-A2 or sSod-A2. <br />Our ongoing study of population structure in razorbacks is <br />limited to non-lethally sampled tissues (muscle and fin), which <br />means that Ck-A and mIcdh-A (both from muscle) could be studied <br />but that Gpi-A2 (expressed in brain) and sSod-A2 (expressed in <br />liver) could not be studied. The first part of our study <br />included a rigorous examination of enzyme expression that <br />employed many buffer systems. This effort identified two more <br />marker loci: mitochondrial malate dehydrogenase (mMdh-A1) and <br />adenosine deaminase (Ada-A2). mMdh-A1 was identified as non- <br />diagnostic by Buth et al. (1987), however a different (obviously <br />non-optimal) buffer was employed in the earlier study. The study <br />of ADA products is often made difficult by the labile nature of <br />the enzyme; it often loses activity rapidly upon frozen storage. <br />PRELIMINARY DATA <br />The original set of tissues sent to us included 13 specimens <br />from Etter Pond (and a few additional specimens identified as <br />hybrids). All thirteen specimens were either heterozygous for <br />razorback and flannelmouth alleles at Ck-A or homozygous for the <br />flannelmouth allele at this locus (Table 1). As found by Buth et <br />al. (1987), this high level of introgression was not matched at <br />the other diagnostic loci. Some additional introgressive <br />heterozygosity was revealed at mMdh-A1, but none at mIcdh-A or <br />Ada-A2. Whereas introgression at the Ck-A locus is evident in <br />all populations of razorbacks, it is at a very low level compared <br />1