The meiotic mutant c(3)G (crossover suppressor on 3 of Gowen) abolishes bot
h synaptonemal complex (SC) formation and meiotic recombination, whereas mu
tations in the mei-W68 and mei-P22 genes prevent recombination but allow no
rmal SC to form. These data, as well as a century of cytogenetic studies, s
upport the argument that meiotic recombination between homologous chromosom
es in Drosophila females requires synapsis and SC formation. We have cloned
the c(3)G gene and shown that it encodes a protein that is structurally si
milar to SC proteins from yeast and mammals. Immunolocalization of the C(3)
G protein, as well as the analysis of a C(3)G-eGFP expression construct, re
veals that C(3)G is present in a thread-like pattern along the lengths of c
hromosomes in meiotic prophase, consistent with a role as an SC protein pre
sent on meiotic bivalents. The availability of a market for SC in Drosophil
a allowed the investigation of the extent of synapsis in exchange-defective
mutants. These studies indicate that SC formation is impaired in certain m
eiotic mutants and that the synaptic defect correlates with the exchange de
fects. Moreover, the observation of interference among the residual exchang
es in these mutant oocytes implies that complete SC formation is not requir
ed for crossover interference in Drosophila.