Erika Bach

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Erika Bach

Associate Professor, Department of Biochemistry and Molecular Pharmacology
Biochemistry and Molecular Pharmacology

Contact Info

Address
550 First Avenue
New York, NY 10016

212/263-5963
Erika.Bach@nyumc.org


Education

— Dr. Bach was a postdoctoral fellow in the Genetics Department at Harvard Medical School., PostDoctoral Training
— Dr. Bach received her Ph.D. in Immunology from Washington University in St. Louis., Graduate Education

Research Summary

1. How does the JAK/STAT pathway regulate stem cells numbers? Regulating the number of stem cells is a primary mechanism by which homeostasis is maintained and oncogenesis is prevented. Stem cells divide to produce daughter cells that renew the stem cell pool or that regenerate tissue by differentiating. The choice between self-renewal and differentiation must be tightly controlled as increasing the stem cell pool provides a condition for oncogenesis. Tumors have cancer stem cells that self-renew and establish new tumors at low numbers. One of the critical regulators of stem cell numbers in mammals is the JAK/STAT pathway. Furthermore, dominant-active mutations in jak and stat genes cause cancer, and Stat3 is a target for therapeutic intervention since its ablation blocks the growth of human cancer cells. Despite these compelling observations, the mechanisms utilized by this pathway to regulate stem cell numbers in mammals have not yet been elucidated, in part due to the redundancy of 4 jak and 7 stat genes. Drosophila provides an ideal system to study how JAK/STAT signaling regulates stem cell numbers, as this function is conserved in several Drosophila tissues, including testis and eye. Unlike the redundancy of the mammalian system, Drosophila has only one jak and one stat gene (called stat92E), which allows facile in vivo analysis. Despite these advantages, nothing is known mechanistically about how this pathway controls stem cell populations in Drosophila. Previous work has shown that over-expression of the cytokine Unpaired, which activates JAK/STAT signaling, leads to an expansion of stem/progenitor cells in the eye and testis. We find that these overgrowths depend on activation of Stat92E within stem cells. Our current hypothesis is that Stat92E must regulate three distinct processes in stem cells in order to regulate their numbers: it must increase cellular mass and accelerate cell cycle progression and, after mitosis, promote self-renewal in some daughter cells. Since Stat92E is a transcription factor, discrete Stat92E target genes should mediate its effects on these processes. We have identified several genes with human homologs that may lie directly downstream of Stat92E and may regulate self-renewal, cellular growth and cell cycle in stem cells.

Research Interests

JAK/STAT signaling; cancer; stem cell self renewal; development|JAK/STAT signaling; cancer; stem cell self renewal; development|JAK/STAT signaling; cancer; stem cell self renewal; development|JAK/STAT signaling; cancer; stem cell self renewal; development

JAK/STAT pathway dysregulation in tumors: A Drosophila perspective
Amoyel, Marc; Anderson, Abigail M; Bach, Erika A
2014-04-24; 1084-9521,Seminars in cell & developmental biology - id: 895872, year: 2014 REVIEW

Cell competition: how to eliminate your neighbours
Amoyel, Marc; Bach, Erika A
2014-02-24; 0950-1991,Development - id: 811212, year: 2014 Journal Article

Neutral competition of stem cells is skewed by proliferative changes downstream of Hh and Hpo
Amoyel, Marc; Simons, Benjamin D; Bach, Erika A
2014-08-10; 0261-4189,EMBO journal - id: 1105342, year: 2014 JOURNAL ARTICLE

Hedgehog is required for CySC self-renewal but does not contribute to the GSC niche in the Drosophila testis
Amoyel, Marc; Sanny, Justina; Burel, Michael; Bach, Erika A
2012-12-17; 0950-1991,Development - id: 202312, year: 2013 Journal Article

JAK/STAT signaling is required for hinge growth and patterning in the Drosophila wing disc
Ayala-Camargo, Aidee; Anderson, Abigail M; Amoyel, Marc; Rodrigues, Aloma B; Flaherty, Maria Sol; Bach, Erika A
2013-10-21; 0012-1606,Developmental biology (Orlando) - id: 573822, year: 2013 Journal Article