Chromosome rearrangements associated with B-A translocations
--Lin, B-Y, Chang, S-J

During the RFLP analysis of hypoploids of four B-A translocations, unexpected results were observed. The hypoploids--identified by their short stature in comparison to the normal sibs, 50% pollen sterility, and chromosome counting--were produced after crossing B73 with pollen of the B-A translocation-carrying L289. The hypoploid gives or lacks the paternal L289 signal following hybridization with RFLP markers, depending on the markers being proximal or distal, respectively, to the breakpoint of the relevant B-A translocations. Most markers show the expected signal pattern on hypoploids, but some do not.

The unexpected results are associated with the hypoploids of three translocations (TB-1Sb, TB-9Sd, and TB-9Lc), exhibiting two different paternal signals: L289 or non-L289. For example, the hypoploid of TB-1Sd, following hybridization with umc177a, gave two signals: B73 and non-L289 (Tables 1 and 2; Lin and Chang, MNL, this volume). The L289 signal is not present. The non-L289 signal is paternal in origin, since it is absent in B73 and in the hybrid between B73 and L289 included in the same analysis. umc177a is the only marker showing the paternal non- L289 signal; other markers flanking umc177a exhibit the expected L289 signal. The same situation was observed in the hypoploids of TB-9Sd and TB-9Lc. In the case of the hypoploids of TB-9Sd, four markers (bnl5.04, umc114, bnl8.17, and umc95) on 9L, show the paternal non-L289 signal. For the hypoploid of TB-9Lc, three markers (bnl3.06, umc247, and umc81) behave similarly. The size of the paternal non-L289 signals is variable: three are larger than the L289 signal, and five others are smaller.

The simplest explanation for the presence of the paternal non-L289 signal is the existence of a chromosome rearrangement--most likely an inversion-- on the A-B chromosome of the three B-A translocations. This explanation is consistent with the fact that markers giving the paternal non-L289 signals are linked together: Four markers of this nature on 9L, spanning over a region of about 19 map units, are closely linked; and three others on 9S, covering about 15 map units, are likewise linked. The affected regions are not interrupted by markers that show the L289 signal.

Also consistent with the explanation is the existence of markers which lack the paternal signal (L289 or non-L289) on hypoploids of the two B-A translocations involving the two arms of the same chromosome. For example, the affected region on the 9-B chromosome is closely associated with bnl5.10, which is deficient for the paternal signal of the hypoploids of TB-9Sd and TB-9Lc (see Table 1; Lin and Chang, MNL, this volume). Since the former carries the deficiency of 9S and the latter the deficiency of 9L, the paternal signal is expected to be absent on only one of the two hypoploids. The fact that it is also absent on the second hypoploid suggests the occurrence of a complex rearrangement that leads to the formation of a chromosome deletion covering the bnl5.10 locus. In addition, since the locus is linked to the three markers on 9S that give the paternal non-L289 signal--no marker giving the L289 signal is located between them, these four markers must be involved in the same rearrangement: bnl5.10 is deleted by an additional breakage before ligation. Accordingly, bnl5.10 is closely linked and proximal to umc81, the most proximal marker of the rearrangement. By the same rationale, umc67 and umc177a are involved in the same rearrangement, and the former, being proximal to the latter, has been deleted from the rearranged region by a similar event.

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