TABLE 2

Summary of CSHJ phenotypes in mutants

AlleleCSHJaRTGbFunction of wild-type gene product in meiosisc
DSB formation and axial element structure
spo11ΔI+++DSB formation; meiotic S-phase regulation
spo11-Y135FI+++Spo11 catalytic residue
rec104ΔI+++Meiotic DSB formation
red1ΔI+++Axial element component; homolog partner choice
hop1ΔI+++Axial element component; homolog partner choice
mek1ΔI++++Checkpoint control kinase; homolog partner choice
hop2ΔI+++Homolog partner choice; interacts with Mnd1
mnd1ΔI++Homolog partner choice; interacts with Hop2
DSB processing and strand invasion
sae2ΔI+d+Removal of Spo11 from DSB; 5′-end resection of DSB
rad55ΔI+++ePromotes Rad51–ssDNA filament formation
dmc1ΔI+++RecA homolog; strand invasion; interacts with Rdh54
rad51ΔI++RecA homolog; strand invasion; interacts with Rad55
rdh54ΔII++Swi/Snf homolog; interacts with Dmc1
rad54ΔIII+++Swi/Snf homolog; interacts with Rad51
Stabilization of strand invasion and recombinant product formation
zip3ΔII+++Component of synapsis initiation complex; promotes CR formation
mer3ΔII+++DNA helicase; promotes CR formation
zip1ΔIII−+++Transverse element of synaptonemal complex; promotes CR formation
zip2ΔII+++Component of synapsis initiation complex; promotes CR formation
ndj1ΔII+++Required for meiotic telomere reorganization and efficient recombination
msh4ΔIII+++MutS homolog; promotes CR formation; interacts with Msh5
msh5ΔIII+++MutS homolog; promotes CR formation; interacts with Msh4
mus81ΔIII+++Required for a subset of CR products arising via SDSA
Additional genes
ime2ΔId+++Entry into meiosis
msc1ΔIII+++Inhibits sister chromatid exchange?; genomic stability
sgs1ΔIId+++RecQ helicase: suppressor of crossing over?
srs2ΔIII+DNA helicase; disrupts Rad51 presynaptic filament in vitro
ris1ΔIII−+++Antagonist of silencing; interacts with Dmc1
dot1ΔIII−+++Histone methytransferase; telomere position effect
dhc1ΔIII+++Dynein heavy chain; microtubule motor
tub3ΔIII+++α-Tubulin (partially redundant function with Tub1)
mlp2ΔIII+++Myosin-like protein; nuclear pore; telomere-length regulation
  • SDSA, synthesis-dependent strand annealing.

  • a Categories correspond to the level of allelic collisions observed: I, spo11Δ-like levels; II, intermediate levels; III, wild-type levels of allelic collision (CSHJ). “+” and “−” indicate slight increases or decreases from the category listed. Quantitative time courses for these single mutants are reported in this work, Peoples et al. (2002), and Peoples-Holst and Burgess (2005).

  • b Return-to-mitotic-growth phenotype: “+++” indicates wild-type levels of RTG viability; “++” indicates some defect (20–50% inviability by t = 10 hr); “+” indicates a relatively strong RTG defect of >50% inviability by t = 10 hr. These phenotypes may differ when compared to NDT80 strains.

  • c References for functional roles are cited in this work, Peoples et al. (2002), and Peoples-Holst and Burgess (2005).

  • d Slight increase in ectopic collision levels.

  • e Transient RTG inviability.