Programs and Activities Highlights
- International Mouse Phenotyping Consortium Network Call
An ORIP staff member presented an NIH update on new approach methodologies (NAMs) and the use of animals in research at the International Mouse Phenotyping Consortium (IMPC) network call on August 12, 2025. The IMPC monthly call includes members of the IMPC, as well as NIH staff. ORIP’s presentation was devoted to the current NIH policies regarding use of animals in research, as well as NAM initiatives. Attendees discussed implementation of the policies and their potential effect on Knockout Mouse Project/IMPC activities.
- Cryopreservation Workshop, Session V: Long-Term Preservation Methods for Nonhuman Primate Models in Biomedical Research
ORIP hosted the Cryopreservation and Other Preservation Approaches for Animal Models Workshop to address topics related to cryopreservation and other preservation methods. Session V, held on July 15, 2025, focused on long-term preservation of nonhuman primate models for biomedical research. This session brought together experts in the field to discuss current state-of-the-art techniques, as well as challenges and barriers in the field. A summary of the workshop will be posted on the ORIP website.
- Wonderous Worms: Unearthing New Insights Into Health
NIH News in Health published an article titled “Wonderous Worms: Unearthing New Insights Into Health” in July 2025. This article included quotes from Dr. Ann Rougvie, an expert in Caenorhabditis elegans biology and principal investigator of the ORIP-supported Caenorhabditis Genetics Center. The article was reviewed by three ORIP grantees: Drs. David Hall, Nathan Schroeder, and David Sherwood.
- Notice of Extension of the Expiration Date for RFA-OD-22-013, Resource-Related Research Projects for Development of Animal Models and Related Materials (R24, Clinical Trials Not Allowed)
ORIP published a notice to extend the expiration date for RFA-OD-22-013, Resource-Related Research Projects for Development of Animal Models and Related Materials (R24, Clinical Trials Not Allowed). RFA-OD-22-013 now expires on September 26, 2025. ORIP’s intent with this funding opportunity is to support resource-related research projects that are aimed at developing and characterizing new resources; improving existing resources; or acquiring deep understanding of a model system to improve the utilization, accessibility, and translational values of models to the research community.
- International Mouse Phenotyping Consortium–Knockout Mouse Phenotyping Project Annual Fall Meeting
The International Mouse Phenotyping Consortium–Knockout Mouse Phenotyping Project (KOMP) Annual Fall Meeting was held on September 15–16, 2024. An ORIP staff member monitored overall project progress and exchange of scientific knowledge of the international collaboration, contributed to the discussions, conducted an in-depth review of the data provided, and crafted meeting conclusions. The meeting conclusions were communicated to the NIH KOMP Working Group and ORIP and DPCPSI leadership.
Read more in the archive.
ORIP-Supported Research Highlights
- Polyploidy Promotes Transformation of Epithelial Cells into Nonprofessional Phagocytes
Removing dead and damaged cells is important for keeping organisms healthy. Under stressful conditions, such as food scarcity, infection, or temperature changes, unnecessary cells can be removed to save energy and maintain balance. Phagocytes are immune cells that remove invading microbes, foreign material, and damaged or dead cells. Specific cells like macrophages act as phagocytes, but other cells, called nonprofessional phagocytes (NPPs), also can take on this role if needed. NPPs need to change from an immature to mature state and undergo activation before they can clear dead and damaged cells. However, the molecular and cell pathways that cause the transitions and activation of NPPs are not well understood. Researchers used fruit flies to study the transition and activation of NPPs. They found that in fruit flies, certain cells in the ovaries can become NPPs capable of removing dead cells during egg development, which is triggered by a signaling pathway called Notch. This process involves the cells multiplying their chromosome sets to more than two, a cell state called polyploidy. Then, the polyploid cells activate JNK signaling, which helps them engulf and remove the dead cells. This research suggests the importance of polyploidy for NPPs to function properly and maintain health during stress.
- Phage-Displayed Synthetic Library and Screening Platform for Nanobody Discovery
Nanobodies are tiny, stable antibodies (a protein that binds to a specific antigen and helps the immune system destroy it) from camels that are valuable in research and medicine. Traditionally, creating nanobodies requires immunizing camels, which is expensive and time consuming. In this study, researchers described the development of a high-throughput screening method for nanobodies using a synthetic library displayed on phages (viruses that infect bacteria). They tested this method by screening for nanobodies that target various secreted proteins found in fruit flies. The identified nanobodies worked well for applications like immunostaining (labeling a specific protein in a sample on a microscope slide) and immunoblotting (a technique that measures the amount of protein in a sample using an antibody). The synthetic library used in this study is now available for nonprofit use, facilitating the development of high-quality nanobodies for biomedical research and therapeutic development.
- PLAA/UFD-3 Regulates P-bodies Through Its Intrinsic Disordered Domain
Maintaining protein balance in cells is essential for survival and adapting to new environments in all species. In eukaryotes (organisms that have a membrane-bound nucleus, from yeast to humans), this balance is controlled through different stages, such as making proteins, modifying them, and breaking them down. The phospholipase A2 activating protein (PLAA) is a protein found in all eukaryotes that helps sort and degrade proteins through interactions with other molecules. However, its exact targets and interactions are not well understood. Researchers studied PLAA in nematode worms and discovered it has a unique role in cellular processing bodies, called P-bodies, that process cytoplasmic mRNA (molecules that carry the genetic information to make proteins). PLAA interacts with another protein, DCAP-1, which helps process mRNA. This study suggests that PLAA forms a complex with DCAP-1 to regulate protein balance in two ways: breaking down proteins and managing mRNA in P-bodies.
- Estimating Realized Relatedness in Free-Ranging Macaques by Inferring Identity-by-Descent Segments
Biological relatedness is a key consideration in studies of behavior, population structure, and trait evolution. Except for parent–offspring dyads (pairs), pedigrees (diagrams that show family member relationships) do not capture individual relatedness perfectly. The number and length of identity-by-descent (IBD) segments of DNA yield the most precise estimates of being related. The researchers used different methods to estimate IBD segments in free-ranging rhesus macaques (both sexes included). Then, they compared the IBD-based estimates to current methods, such as pedigree. The results show that IBD-based estimates are more reliable and provide more detailed information about relations. Future population studies can use this accurate method to investigate predictors and consequences of being genetically related.
- Structural and Functional Basis of Mechanosensitive TMEM63 Channelopathies
Mechanotransduction occurs when cells sense changes in outside physical forces and convert them into electrical or chemical signals. To complete this process, certain ion channels, such as transmembrane protein 63A (TMEM63A), are used to pass ions and fats across cell membranes. TMEM63B and TMEM63C are part of the same protein family as TMEM63A. Mutations in these three channels cause neurodevelopmental disorders. Researchers identified the changes in protein structure and function for common TMEM63A and TMEM63B mutations. The results provide insight into TMEM63 channel dysfunction.
Read more in the archive.
