Our dataset represents a valuable and solid base for further research investigating the molecular mechanisms involved in oyster gonad differentiation and development. The actual in vivo function of the new candidate genes potentially involved in sex differentiation will obviously require the Benzethonium Chloride development of gene knock-down strategies such as RNA interference, a functional assay that was recently found to operate in oyster. Then, we identified statistically significant differentially expressed transcripts within male and female time-course. A one-way ANOVA parametric test was used to investigate the significance of the factors stage and sex using a p-value cut-off of 0.01 and an adjusted Bonferroni’s correction using TMeV 4.6.0 software as previously described. Folinic acid calcium salt pentahydrate cluster analysis was employed to further demarcate the expression patterns occurring during gonad development. Hierarchical clustering and K means clustering were performed using TMeV on the statistically significant transcripts described previously to cluster transcripts based on similarity of expression between oyster gonads. Hierarchical clustering was used to group experimental samples together based on similarity of the overall experimental expression profiling. Gene expression localization was inferred from the results of a student’s T test with a p-value exceeding 99% confidence and an adjusted Bonferroni correction on all 7 stripped stage 3 oocytes samples vs all 4 individuals and 6 pools of stage 3 female gonads using TMeV 4.6.0 software. Programmed Cell death is an evolutionarily conserved cellular process that eliminates unnecessary, damaged, or harmful cells. Inappropriate regulation of this process can lead to developmental disorders, tumorigenesis, or degenerative pathologies in C. elegans, flies, mice, or humans. Molecular and genetic studies in C. elegans have led to the identification and characterization of the evolutionarily conserved genes egl-1, ced-3, ced-4, and ced-9, which constitute the core cell death pathway. The proteins encoded by these genes act in an inhibitory cascade. EGL-1 promotes cell death by antagonizing the cell death inhibitory function of CED-9, a homolog of BCL-2. CED-9 inhibits cell death by antagonizing the Apaf-1-like protein CED-4, which promotes death by activating CED-3. CED-3 belongs to a cysteine protease family known as caspase. It has been proposed that the binding of EGL-1 to CED-9 on the mitochondrial outer membrane transmits a pro-apoptotic signal that results in the CED-4-dependent activation of the cytoplasmic CED-3 caspase, thereby triggering apoptosis. Recent structural evidence suggests that eight CED-4 molecules form a funnel-shaped structure with four-fold symmetry, with each unit being defined by an asymmetric CED-4 dimer. The cavity of this octameric structure provides space for two CED-3 molecules and facilitates their autocatalytic activation. Additionally, the auto-activation of the CED-3 zymogen is negatively regulated by the CED-3 orthologs CSP-2 and CSP-3, which lack caspase activity, revealing that the regulation of CED-3 activity during programmed cell death is complex. Additional factors that regulate the cell killing process during C. elegans development have been reported. MAC-1, an AAA family ATPase, can bind to CED-4 in vitro and prevent programmed cell death. ICD-1 and TFG-1, which are similar to human bNAC and TRK-fused gene, respectively, suppress CED-4-dependent, but CED-3-independent, cell death. In contrast to these cell-death inhibitors, WAN-1, which is a mitochondrial adenine nucleotide translocator and is associated with CED-4 and CED-9 in vitro.