Seongyeol Park^1,2,10, Nanda Maya Mali^3,10, Ryul Kim^1,10, Jeong-Woo Choi^3,4, Junehawk Lee⁵, Joonoh Lim¹, Jung Min Park^3,4, Jung Woo Park⁵, Donghyun Kim^3,4, Taewoo Kim¹, Kijong Yi¹, June Hyug Choi³, Seong Gyu Kwon³, Joo Hee Hong³, Jeonghwan Youk¹, Yohan An¹, Su Yeon Kim¹, Soo A Oh¹, Youngoh Kwon², Dongwan Hong⁶, Moonkyu Kim⁷, Dong Sun Kim³, Ji Young Park⁸, Ji Won Oh^3,4,9,11 & Young Seok Ju^1,2,11

¹Graduate School of Medical Science and Engineering (GSMSE), Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea. 
²GENOME INSIGHT Inc, Daejeon, Republic of Korea. 
³Department of Anatomy, School of Medicine, Kyungpook National University, Daegu, Republic of Korea. 
⁴Immune Square Inc, Daegu, Republic of Korea. 
⁵Korea Institute of Science and Technology Information (KISTI), Daejeon, Republic of Korea. 
⁶Department of Medical Informatics, College of Medicine, Catholic University of Korea, Seoul, Republic of Korea.
⁷Department of Immunology, School of Medicine, Kyungpook National University, Daegu, Republic of Korea. 
⁸Department of Pathology, Kyungpook National University Chilgok Hospital, School of Medicine, Kyungpook National University, Daegu, Republic of Korea. 
⁹Biomedical Research Institute, Kyungpook National University Hospital, Daegu, Republic of Korea. 
¹⁰These authors contributed equally: Seongyeol Park, Nanda Maya Mali, Ryul Kim. 
¹¹These authors jointly supervised: Ji Won Oh, Young Seok Ju.

Cellular dynamics and fate decision in early human embryogenesis remain largely unknown owing to the challenges of performing studies in human embryos¹. Here, we explored whole-genomes of 334 single-cell colonies and targeted deep sequences of 379 bulk tissues obtained from various anatomical locations of seven recently deceased adult human donors. Using somatic mutations as an intrinsic barcode, we reconstructed early cellular phylogenies that demonstrate (1) an endogenous mutational rate that is higher in the first cell division but decreases to approximately one per cell per cell division later in life; (2) universal unequal contribution of early cells to embryo proper, resulting from early cellular bottlenecks that stochastically set aside epiblast cells within the embryo; (3) examples of varying degrees of early clonal imbalances between tissues on the left and right sides of the body, different germ layers and specific anatomical parts and organs; (4) emergence of a few ancestral cells that will substantially contribute to adult cell pools in blood and liver; and (5) presence of mitochondrial DNA heteroplasmy in the fertilized egg. Our approach also provides insights into the age-related mutational processes and loss of sex chromosomes in normal somatic cells. In sum, this study provides a foundation for future studies to complete cellular phylogenies in human embryogenesis.