About

Jesse Mager is a researcher whose work focuses on mammalian embryogenesis, early development, and gene regulation. His research involves understanding the molecular mechanisms underlying processes such as gastrulation, inner cell mass formation, and lineage specification during early mouse development. Mager's contributions include elucidating the roles of various proteins and complexes, such as mitochondrial ribosomal proteins, exosome components, and transcriptional regulators, in embryonic viability and development. His studies also explore the impact of epigenetic modifications, paternal preconception environmental exposures, and the genetic basis of developmental lethality, contributing to a deeper understanding of the genetic and molecular foundations of mammalian embryogenesis.

Research topics

• Biology
• Genetics
• Medicine
• Cell biology
• Materials science
• Cancer research
• Microbiology
• Biochemistry
• Immunology
• Chemistry
• Nanotechnology
• Andrology

Selected publications

• Dynamic remodeling of epithelial junctions in trophoblast cells of the mammalian blastocyst

  Developmental Biology · 2026-03-20

  articleSenior author
  PublisherDOI

• Onset of embryonic and placental defects coincide in 19 of 22 novel mid-gestation lethal murine knockout lines

  Development · 2026-05-07

  articleOpen access

  The focus on assessing embryo-specific defects in lethal knockout (KO) mouse lines has resulted in an underrepresentation of documented placental abnormalities. Presented herein is a uniform analysis of 22 distinct KO mouse lines that exhibit homozygous lethality in a narrow mid-gestation window. All genes altered by each KO have human orthologs, most are implicated in human disease, yet almost all are understudied. To unravel the role each plays in mammalian development, null embryonic and placental phenotype analysis was performed, and wild type (WT) expression of each KO gene was assessed. While the null phenotype of each KO line falls into two broad embryonic categories, the placental phenotypes are diverse and coincide with the onset of gross embryonic defects. The co-occurrence of null embryonic and placental defect onset coupled with WT gene expression highlights that many could be essential in either the embryo or placenta. This analysis serves to guide mid-gestation placental analysis, underscores the importance of routine analysis of the entire conceptus during mid-gestation lethality, and provides functional annotation for each understudied human ortholog.

  PublisherDOI

• Polymer-siRNA nanovectors for treating lung inflammation

  Journal of Controlled Release · 2025-01-04 · 5 citations

  articleOpen access
  PublisherOA PDFDOI

• A Dapl1 ⁺ subpopulation of naïve CD8 T cells is enriched for memory-lineage precursors

  Science Advances · 2025-08-22 · 1 citations

  articleOpen access

  Memory CD8 T cells provide long-lasting immunity, but their developmental origins remain incompletely defined. Growing evidence suggests that functional heterogeneity exists within the naïve T cell pool, shaping lineage potential before antigen stimulation. Here, we identify a subpopulation of naïve CD8 T cells expressing death-associated protein-like 1 (Dapl1) that contains preprogrammed precursors biased toward memory differentiation. The differentiation of these precursors is independent of Dapl1 but relies on the transcription factor B-cell lymphoma/leukaemia 11b (Bcl11b), resulting in the generation of Dapl1 + central memory–like CD8 T cells after infection and stem-like memory cells in cancer. Dapl1 + naïve T cells originate among mature thymocytes and gradually appear in the periphery postnatally. Peripheral Dapl1 + and Dapl1 − populations show limited plasticity, supporting a thymic-imprinting model. These findings reveal a developmentally imprinted subset of naïve CD8 T cells committed to memory fate, uncovering an alternative pathway for memory T cell generation offering new avenues for therapeutic application.

  PublisherDOI

• A Dapl1+ subpopulation of naive CD8 T cells contains committed precursors of memory lineage.

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-02-08 · 2 citations

  preprint

  Memory CD8 T cells play a vital role in providing lasting immune protection, yet their origins remain incompletely understood. Contrary to classical models, emerging evidence suggests that heterogeneity within the naive T cell pool may influence fate decisions prior to antigen encounter. However, the markers of naive T cell heterogeneity have not yet been clearly defined. Here, we describe intraclonal heterogeneity within the naive T cell population marked by the protein Dapl1. Using novel monoclonal antibodies and a reporter-knockout mouse model, we found that Dapl1-positive naive CD8 T cells exhibit distinct phenotypes compared to their Dapl1-negative counterparts. Furthermore, this population includes a subset of pre-programmed precursors biased toward memory lineage fate. The differentiation of these precursors is independent of Dapl1 but relies on the transcription factor Bcl11b, resulting in the generation of Dapl1-positive central memory-like CD8 T cells in response to infection, and stem-like memory cells in response to cancer. Notably, naive Dapl1-positive T cells originate in the thymus among mature thymocytes and gradually appear in the periphery within several days after birth. Our findings suggest that committed memory precursors in the Dapl1-positive population may represent an alternative pathway for memory CD8 T cell generation, offering new avenues for therapeutic application.

  PublisherDOI

• Loss of CMTR1 leads to gastrulation failure and early embryonic lethality

  Developmental Biology · 2025-09-01 · 1 citations

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Assessing the placental and embryonic phenotype of 23 novel organogenesis-lethal Knock-Out Mouse Project (KOMP) alleles.

  Placenta · 2024-08-31

  articleOpen access
  PublisherDOI

• TATA-binding associated factors have distinct roles during early mammalian development

  Developmental Biology · 2024-04-07 · 8 citations

  articleOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Loss of KANSL3 leads to defective inner cell mass and early embryonic lethality

  Molecular Reproduction and Development · 2024-05-01 · 2 citations

  articleOpen accessSenior authorCorresponding

  e-Lysine acetylation is a prominent histone mark found at transcriptionally active loci. Among many lysine acetyl transferases, nonspecific lethal complex (NSL) members are known to mediate the modification of histone H4. In addition to histone modifications, the KAT8 regulatory complex subunit 3 gene (Kansl3), a core member of NSL complex, has been shown to be involved in several other cellular processes such as mitosis and mitochondrial activity. Although functional studies have been performed on NSL complex members, none of the four core proteins, including Kansl3, have been studied during early mouse development. Here we show that homozygous knockout Kansl3 embryos are lethal at peri-implantation stages, failing to hatch out of the zona pellucida. When the zona pellucida is removed in vitro, Kansl3 null embryos form an abnormal outgrowth with significantly disrupted inner cell mass (ICM) morphology. We document lineage-specific defects at the blastocyst stage with significantly reduced ICM cell number but no difference in trophectoderm cell numbers. Both epiblast and primitive endoderm lineages are altered with reduced cell numbers in null mutants. These results show that Kansl3 is indispensable during early mouse embryonic development and with defects in both ICM and trophectoderm lineages.

  PublisherOA PDFDOI

• Overlapping peri-implantation phenotypes of ZNHIT1 and ZNHIT2 despite distinct functions during early mouse development

  Biology of Reproduction · 2024-08-28 · 2 citations

  articleOpen accessSenior author

  Mammalian preimplantation development culminates in the formation of a blastocyst that undergoes extensive gene expression regulation to successfully implant into the maternal endometrium. Zinc-finger HIT domain-containing (ZNHIT) 1 and 2 are members of a highly conserved family, yet they have been identified as subunits of distinct complexes. Here, we report that knockout of either Znhit1 or Znhit2 results in embryonic lethality during peri-implantation stages. Znhit1 and Znhit2 mutant embryos have overlapping phenotypes, including reduced proportion of SOX2-positive inner cell mass cells, a lack of Fgf4 expression, and aberrant expression of NANOG and SOX17. Furthermore, we find that the similar phenotypes are caused by distinct mechanisms. Specifically, embryos lacking ZNHIT1 likely fail to incorporate sufficient H2A.Z at the promoter region of Fgf4 and other genes involved in cell projection organization resulting in impaired invasion of trophoblast cells during implantation. In contrast, Znhit2 mutant embryos display a complete lack of nuclear EFTUD2, a key component of U5 spliceosome, indicating a global splicing deficiency. Our findings unveil the indispensable yet distinct roles of ZNHIT1 and ZNHIT2 in early mammalian embryonic development.

  PublisherOA PDFDOI

Recent grants

• Functional Annotation of the Preimplantation Transcriptome

  NIH · $420k · 2014–2017

• Streamline assessment of early lethal phenotypes in the mouse

  NIH · $6.5M · 2015–2025

Frequent coauthors

• Eleonora Condrea

  Rabin Medical Center

  31 shared

• Kimberly D. Tremblay

  University of Massachusetts Amherst

  26 shared

• Y. Avi‐Dor

  Technion – Israel Institute of Technology

  24 shared

• Wei Cui

  University of Massachusetts Amherst

  19 shared

• A. Razin

  12 shared

• Mary C. Wallingford

  11 shared

• Kun Zhang

  Sichuan University

  11 shared

• G. Izak

  9 shared