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During meiotic prophase, sister chromatids are organized into axial element (AE), which underlies the structural framework for the meiotic events such as meiotic recombination and homolog synapsis. HORMA domain-containing proteins (HORMADs) localize along AE and play critical roles in the regulation of those meiotic events. Organization of AE is attributed to two groups of proteins: meiotic cohesins REC8 and RAD21L; and AE components SYCP2 and SYCP3. It has been elusive how these chromosome structural proteins contribute to the chromatin loading of HORMADs prior to AE formation. Here we newly generated Sycp2 null mice and showed that initial chromatin loading of HORMAD1 was mediated by meiotic cohesins prior to AE formation. HORMAD1 interacted not only with the AE components SYCP2 and SYCP3 but also with meiotic cohesins. Notably, HORMAD1 interacted with meiotic cohesins even in Sycp2-KO, and localized along cohesin axial cores independently of the AE components SYCP2 and SYCP3. Hormad1/Rad21L-double knockout (dKO) showed more severe defects in the formation of synaptonemal complex (SC) compared to Hormad1-KO or Rad21L-KO. Intriguingly, Hormad1/Rec8-dKO but not Hormad1/Rad21L-dKO showed precocious separation of sister chromatid axis. These findings suggest that meiotic cohesins REC8 and RAD21L mediate chromatin loading and the mode of action of HORMAD1 for synapsis during early meiotic prophase., Author summary During meiotic prophase, homologous chromosomes undergo pairing/synapsis. HORMA domain-containing proteins (HORMAD1, HORMAD2) localize along unsynapsed chromosome axis and monitor homolog synapsis. However, molecular mechanisms how mouse HORMA domain-containing proteins that do not contain a definitive DNA-binding domain localize to the axis chromosome remains elusive. In particular, because chromosome axis is generated by meiotic cohesins (RAD21L, REC8) and axial element (AE) components (SYCP2, SYCP3), it has been elusive how those chromosome structural proteins contribute to the loading of HORMAD proteins onto the chromosomes. This was due to the unavailability of Sycp2 KO mouse that should allow deep analysis of chromosome dynamics in the complete absence of AE. To solve this issue, in the present study, we newly generated Sycp2 null mice, in which AE structure was completely abolished. This allowed us to assess meiotic cohesins and AE components separately, in terms of their roles on chromatin loading of HORMAD proteins. The most notable among our findings is that the localization of HORMAD1 on the chromatin is initially mediated through meiotic cohesins prior to axis formation. Intriguingly, our genetic study suggests that HORMAD1 in collaboration with meiotic cohesins plays distinct roles in sister chromatid cohesion, homolog synapsis and meiotic recombination during the early meiotic prophase.