The meiotic cell division produces haploid gametes from diploid progenitors by segregating the maternally- and paternally-derived copies of each chromosome. The faithful distribution of homologous chromosomes in meiosis is facilitated in most organisms by the crossovers formed during homologous recombination. Meiotic recombination occurs through the carefully orchestrated repair of programmed DNA double-strand breaks (DSBs) and takes place shortly after DNA replication during an extended gap phase referred to as meiotic prophase. Both the formation and faithful repair of meiotic DSBs into crossover recombinants requires the large-scale reorganization of each meiotic chromosome into a series of chromatin loops emanating from a central, condensed axis 
. Pre-meiotic S phase (meiS) is longer than pre-mitotic S phase (mitS) in many organisms 
, and it has been hypothesized that the protracted DNA synthesis either contributes to, or is affected by, the dramatic chromosome reorganization that occurs during meiotic prophase.
The kinetics of genome duplication are determined by where and when DNA replication begins. In eukaryotic genomes, DNA replication initiates from many sites along each chromosome, termed origins of replication, whose likelihood of utilization modulates the length of S phase in different developmental situations 
. In yeast, potential replication origins are selected during G1 phase by the loading of the Mcm2-7 replicative helicase at specific sites along each chromosome 6
. Upon entry into S phase, the activities of cyclin-dependent kinase (CDK) and Dbf4-dependent Cdc7 kinase (DDK) trigger the initiation of DNA replication from a subset of these potential origins 
. The remaining “inactive” origins are passively replicated by forks derived from nearby origins. Studies of individual DNA molecules revealed that the time at which each origin initiates DNA replication during S phase varies substantially between cells, and there is little correlation between distant loci, suggesting origin activation is not coordinated 
. Nevertheless, when the population as a whole is considered, a robust and reproducible replication timing program is seen, regardless of strain background or method used to assess replication timing 
, suggesting chromosomal DNA replication can be accurately described by a probability function.
MeiS in budding yeast has been estimated to last between 1.5–3 times as long as mitS 
. Theoretically, the longer duration of meiS could be due to either reduced efficiency of the initiation of DNA replication (from all or a subset of origins), reduced replication fork rates or a combination of both. Previous studies suggested that the extended length of meiS is not due to changes in origin selection because the majority of the origins on chromosomes III and VI initiate DNA replication during both mitS and meiS in budding yeast 
, and genome-wide analyses suggested that origin selection is also similar in both S phases in fission yeast 
In budding yeast there is no clear separation of meiS and the start of prophase; DNA synthesis occurs concurrently with the loading of factors required for axis and DSB formation, and both require the same cell-cycle kinase activities. The meiosis-specific cohesin complex containing Rec8 is loaded onto chromosomes as cells enter meiS, and subsequently the axial proteins Hop1 and Red1 associate with the same axial core sites along each chromosome 
. As cells progress into prophase, chromosomes condense into a characteristic form, with a shortened axis and intervening DNA loops emanating away from the central core (reviewed in 
). Association of both axial and DSB factors with core sites is critical for the formation of DSBs on the adjacent loops by the topoisomerase-like enzyme Spo11 
, whose proper association is dependent on Rec8 
. A possible link between axis morphogenesis and S phase length was inferred from FACS analysis of total DNA content in yeast strains lacking Rec8 and Spo11 
, and conversely, DNA replication timing has been implicated as a determinant of the time of DSB formation 
To better understand how the early meiotic cell division is coordinated, we characterized the kinetics and requirements of meiS and axis formation genome-wide in budding yeast. We found that origin firing was either delayed or less efficient at the majority of origins in meiS. Consistent with a decreased replication capacity, cells were more sensitive to nucleotide depletion during meiS. However, preventing meiotic chromosome reorganization had little effect on origin activation in meiS, suggesting that DNA replication is not strongly regulated by or linked to axis structure. Conversely, full DNA replication was not required for either axis assembly or DSB formation. Together, these data indicate that DNA replication and the initiation of homologous recombination are separable events, which coordinately contribute to the formation of meiotic recombinant chromosomes.