Fig 1: LSM1 modulates the pronucleus-specific localization of HP1ß, ATRX, H3.1/3.2, and H3.3.a Volcano plot showing differentially expressed genes between Ctrl and Lsm1_KD zygotes. Red dots represent upregulated genes in Lsm1_KD zygotes compared with control zygotes, and blue dots represent downregulated genes. Adjusted p-values (two-sided) attained by the Wald test are corrected for multiple testing using the Benjamini and Hochberg method by default (n = 2 biologically independent samples). b GSEA plot showing preferential upregulation of the ncRNA processing pathway and downregulation of the cell cycle processing pathway following Lsm1 KD. c qPCR validation of H3K9me3 modification-related genes and H3 genes in Lsm1_KD zygotes. The statistical data are expressed as mean ± SEM, ns means not significant by two-sided Student’s t test for each comparison, Suv39h2 (p = 0.7478), Hp1ß (p = 0.3525), Atrx (p = 0.8270), H3.1/3.2 (p = 0.6474), H3f3a (p = 0.8779), H3f3b (p = 0.5152). Each reaction for qPCR analysis contains 3 biological replicates, with each replicate from 50 zygotes. d Immunostaining for HP1ß, ATRX, H3.1/3.2, and H3.3 in representative pronucleus and fluorescence intensity analysis of Ctrl and Lsm1_KD zygotes. Scale bars, 20 µm. Representative images from 3 biological replicates, with each replicate containing at least 5 zygotes. The statistical data are expressed as mean ± SEM, *p < 0.05 and ns means not significant by two-sided Student’s t test for each comparison, HP1ß: male p = 0.0340, female p = 0.5630, ATRX: male p = 0.0410, female p = 0.4592, H3.1/3.2: male p = 0.0128, female p = 0.7540 and H3.3: male p = 0.0394, female p = 0.8779. Each treatment contains 3 biological replicates, with each replicate containing at least 5 zygotes.