It was previously shown that in strains ofBacillus subtilis bearing the trpE26 mutation a chromosome segment (from trpD to ilvA) is translocated to a position near the thr region. Further PBS1-mediated transduction data have now revealed that these strains also possess an inversion of part of the chromosome from the origin of replication, down to the tre locus on one side and the cysB locus on the other. These data concern evidence oflinkage oftre-12 to markers in the translocation (hisH2, tyrAl, and metB3) as well as linkage of the cysB3 marker to thi-86, gly-133, and catA. They explain the previously observed absence of linkage of markers in the translocated segment to cysB3. The model proposed for the formation of merodiploids in trpE26 strains, which calls for the fusion of two genetic elements, is not incompatible with this new finding. Moreover, the model was found to be of more general significance. Evidence is presented that merodiploids may also be produced from 168 recipients and trpE26 donors by transduction, when selection is made for particular markers. The markers should be in the ilvA and thr regions. They are widely separated in the recipient 168 strain but are closely linked in the trpE26 donor as a result of the translocation. The diploids so produced are unstable, sensitive to L-lysine, and segregate rapidly.Strains of Bacillus subtilis carrying the trpE26 mutation possess certain properties which distinguish them from those of 168 origin (1, 2, 3). The most important ofthese features is their aptitude to give rise to merodiploid clones when transformed or transduced to tryptophan independence.In a recent paper we have shown that the trpE26 marker is the result ofthe translocation of a chromosome segment (12). The relevent evidence was obtained by studies on the replication order of markers, using the density transfer technique, and from the results of mapping experiments. Markers on a chromosome segment extending from trpD to ilvA replicated earlier in trpE26 strains, at about the same time as tre-12 and thr-5. These two markers (the replication times of which are close in strain 168) are situated on opposite sides of the bidirectionally replicating chromosome (5,9,14). Those markers normally flanking the region (trpE8 and citK7) replicated late, as usual. The results suggested that the trpD-ilvA segment was shifted in strains bearing the trpE26 marker to a position closer to the origin of replication, near tre or thr. Mapping experiments by PBS1 transduction, when both donor I Present address: Department of Microbiology, Scripps Clinic and Research Foundation, La Jolla, Calif. 92037. and recipient carried the trpE26 marker, clearly showed that the segment was removed from its normal position to a site near thr (i) aroB2 and citK7 were linked in these strains;(ii) linkage of cysB3 and thr-5 was lost; (iii) several markers in the translocation were linked to thr-5 and ald. However, similar transduction crosses failed to reveal linkage of the translocation to cysB3. These negative results hav...