Doctor of Philosophy (Ph.D.)
Biology
Johns Hopkins University
2007
Anna Krueger Allen, Ph.D., is an associate professor in the Department of Biology at Howard University. She earned her Ph.D. in Biology from Johns Hopkins University and her B.S. in Biology and Environmental Studies, summa cum laude, from The George Washington University. Prior to joining Howard University, she completed postdoctoral research at the National Institutes of Health and the Carnegie Institution for Science and served as a Visiting Research Scientist at the National Institutes of Health.
Allen’s research focuses on the molecular and cellular mechanisms that regulate oocyte quality, fertility, and early embryonic development. Using Caenorhabditis elegans as a model organism, her work examines germline development, meiosis, and cell cycle regulation. Her research has been supported by funding from the National Institutes of Health and the Department of Defense and has been published in leading peer-reviewed scientific journals.
In addition to her research, Allen is committed to undergraduate and graduate education and mentorship in the biological sciences. She teaches courses in general biology, genetics, and developmental biology and incorporates inquiry-based learning and course-based undergraduate research into her teaching. Through her scholarship, teaching, and service, she contributes to advancing biological research and training the next generation of scientists.
Biology
Johns Hopkins University
2007
Biology and Environmental Studies
George Washington University
2001
Currently Active Research Funding:
Department of Defense Research Award (2018-2022)
Completed Research Funding:
National Institutes of Health R15 Award (2016 - 2021)
DOD Major Research Instrumentation - Spinning Disk Confocal Microscope (2013)
Research summary
The overall goal of the Allen lab is to study the mechanisms by which a high quality gamete (the egg) is generated and how that gamete then undergoes one of the most fascinating process in development, fertilization. We use the nematode C. elegans as a model system to study two specific aspects of meiosis: 1) oocyte meiotic arrest and 2) oocyte maturation. To address these issues, we are taking an interdisciplinary approach involving genetics, molecular biology, cytological and biochemical techniques to study C. elegans meiosis.
Currently the lab is working on studying the role of an RNA-binding protein (ETR-1) in oogenesis and also on elucidating a potential non-canonical, non-proteolytic role for subunits of the proteasome in reproduction.
Lab Personnel
Lourds Michelle Fernando (graduate student)
Benedict Quagraine (gradute student)
Caroline Ugoaru (undergraduate student)
Jeandele Elliot (undergraduate student)
Comparison of N- and C-terminally endogenously GFP-tagged WEE-1.3 strains in C. elegans
We have generated a WEE-1.3 strain in C. elegans where we have endogenously tagged the C-terminus with GFP. In this publication we demonstrate that this new strain exhibits the same expression localization pattern as the WEE-1.3 antibody and N-terminally endogenously GFP-tagged WEE-1.3 strain that have been previously published. We also show for the first time that endogenously tagging WEE-1.3 at either termini does not affect the reproductive function of the worms.
The proteasome is a multi-subunit complex and a major proteolytic machinery in cells. Most subunits are essential for proteasome function, and depletion of individual subunits normally results in lethality. RPN-12/Rpn12/PSMD8 is a lid subunit of the 19S regulatory particle (RP) of the 26S proteasome. Studies in Caenorhabditis elegans demonstrated that RNAi depletion of RPN-12 does not result in lethality. RPN-12 has not been well studied in higher eukaryotes. In this study, we investigate the biological significance of RPN-12 in C. elegans. We found that the null mutant rpn-12(av93) did not cause major impairment of the proteolytic activity of the proteasome.
Our data suggests that RPN-12 is not essential for viability and lifespan of C. elegans under normal conditions (20ºC), but that absence of RPN-12 can result in a significant increase in mean lifespan under heat stress (25ºC).
A hallmark of the research experience is encountering difficulty and working through those challenges to achieve success. This ability is essential to being a successful scientist, but replicating such challenges in a teaching setting can be difficult. The Genomics Education Partnership (GEP) is a consortium of faculty who engage their students in a genomics Course-Based Undergraduate Research Experience (CURE). Students participate in genome annotation, generating gene models using multiple lines of experience is continuous and recursive, frequently beginning with frustration but eventually leading to success as they come up with defendable gene models.
Undergraduate research experiences (UREs) increase interest in STEM (science, technology, engineering, and mathematics) research and careers. UREs are utilized as recruitment tools for advanced degree programs and often target underrepresented minorities (URMs). However, UREs accommodate a limited number of students. Course-based UREs (CUREs) have the same benefits as UREs and reach more students, but traditionally cannot be used for recruitment. Here we describe and assess a 1-week “miniCURE” for the perceived value of its components and ability to meet course learning objectives, provide similar research benefits, and serve as a URM recruitment tool.
This Primer article is designed to provide essential background information on C. elegans spermatogenesis and the relevant scientific techniques that will assist students and instructors in their understanding and discussion of the related article.
The GEP: Crowd-Sourcing Big Data Analysis with Undergraduates
The era of ‘big data’ is also the era of abundant data, creating new opportunities for student–scientist research partnerships. By coordinating undergraduate efforts, the Genomics Education Partnership produces high-quality annotated data sets and analyses that could not be generated otherwise, leading to scientific publications while providing many students with research experience.
This study sought to further define the precocious maturation phenotype and to identify novel interactors with WEE-1.3. We found that WEE-1.3 is expressed throughout the germline and in developing embryos in a perinuclear pattern, and demonstrated that oocytes in WEE-1.3-depleted germlines have begun to transcribe embryonic genes and exhibit inappropriate expression of proteins normally restricted to fertilized eggs.
Novel functions for the RNA-binding protein ETR-1 in Caenorhabditis elegans reproduction
In this study, we show that ETR-1 is expressed in the hermaphrodite somatic gonad and germ line, and that reduction of ETR-1 via RNA interference (RNAi) results in reduced hermaphrodite fecundity. Detailed characterization of this fertility defect indicates that ETR-1 is required in both the somatic tissue and the germ line to ensure wild-type reproductive levels.
emb-1 encodes the APC16 subunit of the Caenorhabditis elegans Anaphase-Promoting Complex
In the nematode Caenorhabditis elegans, temperature-sensitive mutants of emb-1 arrest as one-cell embryos in metaphase of meiosis I in a manner that is indistinguishable from embryos that have been depleted of known subunits of the anaphase-promoting complex or cyclosome (APC/C). Here we show that the emb-1 phenotype is enhanced in double mutant combinations with known APC/C subunits and suppressed in double mutant combinations with known APC/C suppressors. In addition to its meiotic function, emb-1 is required for mitotic proliferation of the germline. These studies reveal that emb-1 encodes K10D2.4, a homolog of the small, recently discovered APC/C subunit, APC16.
The vertebrate nuclear hormone receptor steroidogenic factor 1 (SF1; NR5A1)controls reproductive development and regulates the transcription of steroid-modifying cytochrome P450 genes. We find that the SF1-related Drosophila nuclear hormone receptor HR39 is also essential for sexual development. In Hr39 mutant females, the sperm-storing spermathecae and glandular parovaria are absent or defective, causing sterility. Our results indicate that spermathecae and parovaria secrete reproductive tract proteins required for sperm maturation and function, like the mammalian epididymis and female reproductive tract.