THE MAIZE DESYNAPTIC1 MUTATION DISRUPTS MEIOTIC CHROMOSOME SYNAPSIS

In most eukaryotes, homologous chromosomes undergo synapsis during the first meiotic prophase. A consequence of mutations that interfere wit h the fidelity or completeness of synapsis can be failure in the Forma tion or maintenance of bivalents, resulting in univalent formation at diakinesis and production of unbalanced spores or gametes. Such mutati ons, termed desynaptic mutations, can result in complete or partial st erility. We have examined the effect of the maize desynaptic 1-9101 mu tation on synapsis, using the nuclear spread technique and electron mi croscopy to examine microsporocytes ranging From early pachytene until the diplotene stage of prophase I. Throughout the pachytene stage, th ere was an average of about 10 sites of lateral element divergence (in dicating nonhomologous synapsis), and during middle and late pachytene , an average of two and three sires of foldback (intrachromosomal) syn apsis, per mutant nucleus, respectively. By the diplotene stage, the n umber of sites of lateral element divergence had decreased to seven, a nd there was an average of one foldback synapsis site per nucleus. lat eral element divergence and foldback synapsis were not found in spread pachytene nuclei from normal plants. These results imply that the nor mal expression of the dsy1 gene is essential for the restriction of ch romosome synapsis to homologues. The abundance of nonhomologous synaps is and the persistence of extended stretches of unsynapsed axial eleme nts throughout the pachytene stage of dsy1-9101 meiocytes suggests tha t this mutation disrupts both the fidelity of homology search and the forward course of the synaptic process. This mutation may identify a m aize mismatch repair gene. (C) 1997 Wiley-Liss, Inc.