Opportunity Information: Apply for PA 16 088
Apply for PA 16 088
- The HHS-NIH11 in the health, income security and social services sector is offering a public funding opportunity titled "Oocyte Mitochondrial Function in Relation to Fertility, Aging, and Mitochondrial Diseases (R01)" and is now available to receive applicants.
- Interested and eligible applicants and submit their applications by referencing the CFDA number(s): 93.865,.
- This funding opportunity was created on Jan 25, 2016 and posted on Jan 25, 2016.
- Applicants must submit their applications by May 07, 2019. (Agency may still review applications by suitable applicants for the remaining/unused allocated funding in 2026.)
- Eligible applicants include: State governments, County governments, City or township governments, Special district governments, Independent school districts, Public and State controlled institutions of higher education, Native American tribal governments (Federally recognized), Public housing authorities/Indian housing authorities, Native American tribal organizations (other than Federally recognized tribal governments), Nonprofits having a 501(c)(3) status with the IRS, other than institutions of higher education, Nonprofits that do not have a 501(c)(3) status with the IRS, other than institutions of higher education, Private institutions of higher education, For profit organizations other than small businesses, Small businesses, Others (see text field entitled Additional Information on Eligibility for clarification).
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Opportunity Summary:
The Oocyte Mitochondrial Function in Relation to Fertility, Aging, and Mitochondrial Diseases (R01) funding opportunity (PA 16-088) is a discretionary grant program from the U.S. Department of Health and Human Services, National Institutes of Health (NIH) (listed as HHS-NIH11). It was posted on January 25, 2016, with an application closing date of May 7, 2019. The program uses the NIH R01 mechanism, meaning it is intended to support substantial, hypothesis-driven research projects led by investigators proposing significant and rigorous scientific aims. The announcement is tied to CFDA numbers 93.865, indicating it sits within NIH health-related research funding streams.
The central focus of the opportunity is the biology of mitochondria in the oocyte (the female egg cell) and how mitochondrial performance influences fertility, reproductive aging, and the risk of transmitting mitochondrial diseases to children. Mitochondria are the cell's energy-producing organelles and also play roles in metabolism, signaling, oxidative stress, and regulation of cell survival. Because early embryonic development relies heavily on maternal stores within the oocyte, mitochondrial quantity and quality in the egg can strongly affect whether fertilization succeeds, whether embryos develop normally, and whether offspring health is impacted long after birth. This FOA is designed to push the field toward deeper, fundamental understanding of what healthy mitochondrial function looks like in oocytes, how and why it declines with age or disease, and what the downstream consequences are for reproduction and child health.
A major stated goal is to generate foundational insight into both the role of mitochondria in the oocyte and the long-term consequences when mitochondrial function is impaired. In practical terms, this can include research that clarifies how mitochondrial DNA integrity, mitochondrial biogenesis, bioenergetic capacity, and oxidative stress responses contribute to oocyte quality and developmental competence. It also emphasizes the need to understand what happens when these systems break down, including how dysfunction could contribute to infertility or subfertility, age-related declines in reproductive potential, and the possibility of passing mitochondrial defects to the next generation.
Beyond basic discovery, the FOA explicitly encourages development of therapeutic or alternative approaches aimed at correcting or mitigating mitochondrial dysfunction. The intent is not simply to describe problems but to move toward strategies that could improve oocyte quality and competency, and ultimately support healthier outcomes for resulting offspring. Depending on the scientific approach, this could involve interventions that restore mitochondrial function, reduce damaging stress signals, improve metabolic homeostasis, or otherwise enhance the oocyte's ability to support fertilization and early development. The announcement frames these efforts as potentially leading to practical approaches for women affected by infertility or subfertility linked to mitochondrial dysfunction, as well as women whose broader health conditions may involve mitochondrial defects that could influence reproductive outcomes.
Eligibility is broad and includes many types of U.S. organizations that commonly apply for NIH grants. Eligible applicants listed include state, county, and city or township governments; special district governments; independent school districts; public and state-controlled institutions of higher education; private institutions of higher education; federally recognized Native American tribal governments; other Native American tribal organizations; public housing authorities and Indian housing authorities; nonprofit organizations with and without 501(c)(3) status (other than institutions of higher education); for-profit organizations (other than small businesses); small businesses; and other entities as described in the FOA's additional eligibility language. This wide eligibility is meant to attract proposals from academic labs, medical centers, research institutes, and potentially industry partners capable of conducting rigorous reproductive biology and mitochondrial research.
Overall, the opportunity is aimed at advancing the science of how mitochondrial function in the oocyte shapes fertility across the lifespan and influences disease risk in offspring, with a clear translational motivation. The NIH expectation, as stated in the description, is that results from funded projects will help produce actionable knowledge and interventions that can enhance fertility and improve the well-being of children born from oocytes affected by mitochondrial dysfunction.
Frequently Asked Questions (FAQs)
What is the name of this funding opportunity?
The funding opportunity is titled Oocyte Mitochondrial Function in Relation to Fertility, Aging, and Mitochondrial Diseases (R01), referenced as PA 16-088.
Which federal agency is offering this grant?
This is a discretionary grant program from the U.S. Department of Health and Human Services (HHS), specifically the National Institutes of Health (NIH) (listed as HHS-NIH11).
What grant mechanism does this program use?
The program uses the NIH R01 mechanism, which is intended to support substantial, hypothesis-driven research projects led by investigators proposing significant and rigorous scientific aims.
When was this opportunity posted?
The opportunity was posted on January 25, 2016.
What is the application closing date?
The application closing date listed is May 7, 2019.
What CFDA number is associated with this opportunity?
This announcement is tied to CFDA 93.865, placing it within NIH health-related research funding streams.
What is the central scientific focus of the FOA?
The FOA focuses on mitochondrial biology in the oocyte (female egg cell) and how mitochondrial performance influences fertility, reproductive aging, and the risk of transmitting mitochondrial diseases to children.
Why are mitochondria in the oocyte important for fertility and early development?
Mitochondria produce cellular energy and also affect metabolism, signaling, oxidative stress, and cell survival. Because early embryonic development relies heavily on maternal stores in the oocyte, the quantity and quality of oocyte mitochondria can influence whether fertilization succeeds, whether embryos develop normally, and whether offspring health is affected long after birth.
What kinds of mitochondrial features or processes does the FOA highlight?
The FOA points to foundational research needs around topics such as mitochondrial DNA integrity, mitochondrial biogenesis, bioenergetic capacity, and oxidative stress responses as contributors to oocyte quality and developmental competence.
What major research goals does the FOA emphasize?
A major goal is to generate foundational insight into (1) the role of mitochondria in the oocyte and (2) the long-term consequences when mitochondrial function is impaired, including impacts on infertility/subfertility, age-related reproductive decline, and potential transmission of mitochondrial defects to the next generation.
Is this FOA strictly basic science, or does it also encourage translational work?
It includes a strong translational motivation. In addition to basic discovery, the FOA explicitly encourages the development of therapeutic or alternative approaches to correct or mitigate mitochondrial dysfunction and improve oocyte quality, competency, and offspring outcomes.
What types of interventions or approaches are encouraged (at a high level)?
Depending on the proposed scientific approach, the FOA describes interest in strategies that could restore mitochondrial function, reduce damaging stress signals, improve metabolic homeostasis, or otherwise enhance the oocyte's ability to support fertilization and early development.
How does the FOA connect mitochondrial dysfunction to infertility and aging?
The FOA highlights that declines in mitochondrial quantity/quality or performance can contribute to infertility or subfertility and age-related declines in reproductive potential, and it seeks to clarify how and why those declines occur.
How does this opportunity relate to mitochondrial diseases in offspring?
It emphasizes understanding the risk of transmitting mitochondrial defects to children and the downstream consequences of impaired mitochondrial function for reproduction and long-term child health.
Who is eligible to apply?
Eligibility is broad and includes many U.S. organization types commonly eligible for NIH grants, including:
- State governments
- County governments
- City or township governments
- Special district governments
- Independent school districts
- Public and state-controlled institutions of higher education
- Private institutions of higher education
- Federally recognized Native American tribal governments
- Other Native American tribal organizations
- Public housing authorities and Indian housing authorities
- Nonprofit organizations with 501(c)(3) status (other than institutions of higher education)
- Nonprofit organizations without 501(c)(3) status (other than institutions of higher education)
- For-profit organizations (other than small businesses)
- Small businesses
- Other entities as described in the FOA's additional eligibility language
What kinds of institutions is NIH trying to attract to apply?
The wide eligibility is meant to attract proposals from academic labs, medical centers, research institutes, and potentially industry partners capable of conducting rigorous research in reproductive biology and mitochondrial function.
What outcomes does NIH expect from projects funded under this FOA?
The NIH expectation described is that funded projects will produce actionable knowledge and potential interventions that can enhance fertility and improve the well-being of children born from oocytes affected by mitochondrial dysfunction.
What does "hypothesis-driven" mean in the context of this R01?
Within this opportunity, the R01 mechanism is described as supporting research led by investigators proposing significant and rigorous scientific aims, consistent with a hypothesis-driven approach where studies are designed to test well-defined scientific questions about oocyte mitochondrial function and its consequences.
Is the focus limited to fertility outcomes, or does it include longer-term health effects?
It includes both. The FOA emphasizes not only fertilization and embryo development, but also how mitochondrial quality in the oocyte may influence offspring health long after birth.
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