Publications by authors named "S S Rajderkar"
Article Synopsis
- * Researchers combined various methods, including histone modification and single-cell analysis, to map out the regulatory elements involved in craniofacial development in both humans and mice.
- * They identified 14,000 human craniofacial enhancers, with over half showing similar chromatin patterns in mice, creating a valuable resource for future genetics and developmental research.
Mouse models are a critical tool for studying human diseases, particularly developmental disorders. However, conventional approaches for phenotyping may fail to detect subtle defects throughout the developing mouse. Here we set out to establish single-cell RNA sequencing of the whole embryo as a scalable platform for the systematic phenotyping of mouse genetic models.
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- The study addresses the unclear genetic factors behind craniofacial birth defects and facial shape variations, focusing on the role of distant-acting transcriptional enhancers in gene regulation during key developmental stages.
- Researchers created a detailed catalogue of around 14,000 enhancers involved in human facial development by combining profiling of histone modifications and chromatin accessibility, along with single-cell analysis, across various embryonic stages.
- The findings reveal that 56% of human craniofacial enhancers are conserved in mice, offering valuable insights for understanding the genetic underpinnings of craniofacial conditions and enhancing future studies in genetics and development.
Background: We estimated the incidence of Japanese encephalitis (JE) and acute encephalitis syndrome (AES) following routine immunization with the live-attenuated SA 14-14-2 JE vaccine.
Methods: We implemented enhanced surveillance of AES and JE hospitalizations in endemic districts in Maharashtra and Telangana States during 2015-2016 and 2018-2020. We estimated incidence and compared differences in the incidence of JE and AES between two states, and vaccinated and unvaccinated districts during two study periods.
Topologically associating domain (TAD) boundaries partition the genome into distinct regulatory territories. Anecdotal evidence suggests that their disruption may interfere with normal gene expression and cause disease phenotypes, but the overall extent to which this occurs remains unknown. Here we demonstrate that targeted deletions of TAD boundaries cause a range of disruptions to normal in vivo genome function and organismal development.
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