The research goal of the Rao Lab is to understand and manage fungal infectious diseases.
Reeta Rao studies the biology of fungal diseases, particularly those caused by Candida, a species of fungi prevalent in humans. These microorganisms cause oral thrush, ear infections, and vaginitis but can also cause systemic infections in immunocompromised individuals. It is a leading cause of serious illnesses and death among hospitalized patients. Although the causes for the recent emergence in clinical settings across the globe are unknown, they likely include new or increasing antifungal selection pressures in humans, animals, or the environment. The high mortality rate is likely related to antimicrobial resistance.
She combines biochemical, molecular-genetic and genomic tools to explore microbial virulence strategies. We use a multiple host models including cultured mammalian macrophages, enteroids or “mini guts” raised in petri dishes from intestinal stem cells, as well as whole animals models such as nematodes and mice to study host immune responses. We also employ high throughput screens to identify novel therapeutics. Ultimately these studies will lead to novel therapeutics for fungal diseases, which are notoriously difficult to treat.
She was elected a fellow of the American Academy of Microbiology in recognition of her excellence, originality, and leadership in the microbiological sciences.
As an academic scientist, Reeta Rao is committed to the professional development of the next generation of Scientists. Preparing them with the right experience and aptitude for a fulfilling career. Since the largest attrition to scientific pool is during undergraduate years, she organizes a research symposium in the greater Boston Area – “Next-in-BIO” that aims to obtain, improve, and retain the skills, knowledge, and resources needed in academia as well as the industry. The goal is to keep young researchers engaged in Science while serving as a capacity development opportunity for the biotech sector.
She has also championed a skill-based MS degree program designed to provide a broad base in advanced coursework and laboratory techniques applicable to the Biotechnology Industry.
She won the Waksman Outstanding Teaching Award from the Society of Industrial Microbiology and Biotechnology in recognition of her contributions to teaching and learning.
The lab has been interested in understanding how pathogens thrive within host immune cells. We trace the fate of single host-pathogen pairs during interaction. We can distinct transcriptional trajectories suggesting that both the host as well as the pathogen are engaged in “bet hedging”. For example, we identify of key genes involved in adaptation to host niches contributes to pathogen fitness. Likewise host genes involved in pathogen recognition suggests processes for therapeutic intervention.
The CDC published a “watch list” of antimicrobial resistant microbes “super bugs”. Among these, fluconazole-resistant Candida was the only fungal species identified as a serious public health threat. More recently, Candida auris, has simultaneously emerged in several countries, as a multi drug resistant fungal pathogen with high mortality rates. One project in the lab is focused on defining the molecular interaction between Candida auris and host immune cells.
Other projects in the lab are focused on understanding microbial interactions in the context of a host. Microbes play an important role in all aspects of human life. For example, Inflammatory bowel disease (IBD), ulcerative colitis and Crohn’s disease are thought to be caused by an imbalance in the intestinal microbiota or inappropriate host immune response. Projects in the lab address basic questions of how beneficial microbes can act as a probiotic against pathogenic microbes and maintain a healthy microbiota, explore mechanisms that disrupt this interaction and cause devastating infections and identify host immune defenses that alter microbial response.
Revealing parallel host-pathogen transcriptional dynamics using sorted subpopulations and single, Candida albicans infected macrophages.
Authors: Muñoz, J F, Delorey, T, Ford, C B, Li, B Y, Thompson, D A, Rao, R P , Cuomo C A.
Source: Nat Commun 10, 1607
Caenorhabditis elegans as a model host to monitor the Candida infection process .
Authors: Elkabti, A,Issi, L, Rao R.
Source: Journal of Fungi.
Emerging pathogens of the Candida species.
Authors: Yang, B,Rao R.
Source: Chapter in book entitled “Candida albicans,” published by IntechOpen, London.
The nematode Caenorhabditis elegans – A versatile in vivo model to study host-microbe interactions.
Authors: Issi, L, Rioux, M, Rao R.
Source: J. Vis. Exp 16(1):41, 128(e56487).
A pretherapeutic coating for medical devices that prevents the attachment of Candida albicans.
Authors: Vargas-Blanco D, Lynn A, Rosch J, Noreldin R, Salerni A, Lambert C, Rao R.
Source: BMC: Ann Clin Microbiol Antimicrob 16(1):41.
Whole genome sequence of the heterozygous clinical isolate Candida krusei 81-B-5.
Authors: Cuomo, C, Shea, T, Yang, B, Rao R, Forche, A .
Source: Jul10, pii:G3.10.1534/g3.117.043547.
Zinc Cluster Transcription Factors alter virulence in Candida albicans.
Authors: Issi L., Farrar RA., Pastor K., Landry B., Delorey T, Bell G, Thompson DA, Cuomo CA, Rao RP.
Source: Genetics, February 2017 205: 559-576.
The mutational landscape of gradual acquisition of drug resistance in clinical samples of Candida albicans.
Authors: Funt JM, Abbey D, Issi L, Oliver BG, White TC, Rao RP, Berman J, Thompson DA, Regev A.
Source: DOI: 10.7554/eLife.00662.002 (2015).
Chemical screening identifies a small molecule inhibitor of C. albicans adhesion, morphogenesis and pathogenesis.
Authors: Fazly A, Jain C, Dehner AC, Issi L, Lilly E, Fidel PL, Rao RP, Kaufman PD.
Source: PNAS 110(33): 13594-13599 (2013).
The role of Candida albicans AP-1 protein against host derived ROS in in-vivo models of infection.
Authors: Jain C, Pastor K, Gonzalez AY, Lorenz MC, Rao RP.
Source:Virulence 4: 67-76 (2012).
Aberrant synthesis of Indole-3-acetic acid in Saccharomyces cerevisiae triggers morphogenic transition, a virulence trait of pathogenic fungi.
Authors: Prusty Rao R, Hunter A, Kashpur O and Normanly J
Source: Genetics 185 (1): 211-220 (2010).
Featured in the highlights section of the journal.
Featured in Faculty of 1000.
A Patho-assay using S. cerevisiae and C. elegans reveals novel roles for yeast AP-1, Yap1 and host dual oxidase BLI-3 in fungal pathogenesis.
Authors: J Charu, Yun M, Politz S. M, Prusty Rao R.
Source: Eukaryotic Cell. 8 (8) 1218-1227 (2008).
Featured in the Science highlights of the NECN Cable News network.
Expression Profiling of Auxin-Treated Arabidopsis Roots: Toward a molecular analysis of lateral root emergence.
Authors: Laskowski M, Biller S, Stanley K, Kajstura T, Prusty R.
Source: Plant and Cell Physiology 47(6): 788-792 (2006).
SCH9, a putative kinase from Saccharomyces cerevisiae, affects HOT1-stimulated recombination.
Authors: Prusty R, Keil RL.
Source: Molecular Genetics and Genomics, 272: 264-274 (2004).
The plant hormone, Indole acetic acid, induces invasive growth in Saccharomyces cerevisiae.
Authors: Prusty R, Grisafi P, Fink GR.
Source: PNAS USA, 101(12): 4153-57 (2004).
Featured in Faculty of 1000 ‘must read papers’
Ribosomal DNA replication fork barrier and HOT1 recombination hot spot: shared sequences but independent activities.
Authors: Ward TR*, Huong MJ*, Prusty R*, Lau CK, Keil RL, Fangman WL, Brewer BJ. (* Equal contribution).
Source: Molecular and Cellular Biology, 20(13): 4948-57 (2000).
Elimination of yeast replication block protein Fob1p extends the life span of mother cells.
Authors: Defossez P, Prusty R, Kaeberlein M, Lin S, Ferrigno P, Silver PA, Keil RL, Guarente L.
Source: Molecular Cell, 3: 447-455 (1999).
Featured in News and Views in Nature Genetics, May 1999, 22: 4-6.
ENOD 8, a Medicago early nodulin gene, expressed in empty nodules.
Authors: Dickstein R, Prusty R, Peng T, Ngo W and Smith ME.
Source: Molecular Plant Microbe Interactions, 6: 715-721 (1993).
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