Genetics and Gene Regulation

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 15 August 2026 | Viewed by 1933

Editors

Institute for Human Genetics, University of California, San Francisco, CA, USA
Interests: genetics; gene regulation; non-coding genome

Special Issue Information

Dear Colleagues,

The gene regulatory network is critical in maintaining diverse cellular functions and higher-order organismal phenotypes. Dysfunction in the regulatory network caused by genetic alterations has been implicated in numerous diseases, including cancers, neurodevelopmental disorders, and neurodegenerative diseases. Large-scale genetic studies, such as genome-wide association studies, and high-throughput genomic studies, such as whole-genome sequencing and whole-exome sequencing, have been pivotal in identifying disease-associated genetic factors. A significant proportion of these factors relate to regulatory elements, underscoring the importance of gene regulation in genetic susceptibility to diseases. However, we are yet to fully understand exactly which factors are involved and how they contribute to human diseases at the molecular level. This Special Issue will explore the latest technological advancements and molecular mechanisms involved in studying the contributions of genetic factors to gene regulation and human diseases. By bridging the gap between genetic discoveries and functional mechanisms, this Special Issue will advance our understanding of genetic contribution in gene regulation and human diseases and provide enhanced strategies for disease diagnosis, prevention, and treatment.

Dr. Yujing Li
Dr. Han Yang
Guest Editors

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Keywords

  • genetics
  • gene regulation
  • human diseases

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Published Papers (1 paper)

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Research

17 pages, 4317 KB  
Article
Natural Genetic Variation Impacts Stress-Induced Quiescence and Regeneration in Response to Rapamycin
by Sahiti Peddibhotla, Miriam Gonzaga, Tricia Zhang, Yasha Goel, Jun Sun, Benjamin R. Harrison, Daniel E. L. Promislow and Hannele Ruohola-Baker
Cells 2026, 15(3), 236; https://doi.org/10.3390/cells15030236 - 26 Jan 2026
Viewed by 1425
Abstract
In response to ionizing radiation (IR), both adult and cancer stem cells enter reversible cell cycle arrest at the G1/S transition to evade apoptosis and subsequently re-enter the cell cycle to regenerate damaged tissue. Entry into and exit from this arrest, known as [...] Read more.
In response to ionizing radiation (IR), both adult and cancer stem cells enter reversible cell cycle arrest at the G1/S transition to evade apoptosis and subsequently re-enter the cell cycle to regenerate damaged tissue. Entry into and exit from this arrest, known as “quiescence,” is governed by the inhibition of mTORC1. The pharmacological suppression of mTORC1 with rapamycin prevents quiescent stem cells from re-entering the cell cycle and impairs tissue regeneration. Rapamycin holds great therapeutic promise in preventing tumor regrowth from dormant cancer stem cells. Yet the extent to which genetic background impacts the known variation in the pharmacological response of rapamycin remains unknown. Here, we show that natural genetic variation across the Drosophila Genetics Reference Panel (DGRP) drives substantial differences in the rapamycin-mediated suppression of post-IR quiescence and regeneration. To define the basis of this differential sensitivity, we examined mitochondrial turnover and DNA damage repair—processes controlling IR-induced dormancy. Our analyses reveal that variation in rapamycin sensitivity is more strongly associated with differences in mitochondrial dynamics than with DNA damage response following radiation. Together, these findings demonstrate that genetic background is a critical determinant of rapamycin efficacy and identify mitochondrial regulation as a key mechanism underlying differential therapeutic response. Full article
(This article belongs to the Special Issue Genetics and Gene Regulation)
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