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Ann Rougvie, Ph.D.

Professor

Mailing Address:
University of Minnesota
Department of Genetics, Cell Biology, and Development
6-160 Jackson
321 Church St. SE
Minneapolis, MN 55455
USA
Education:
Ph.D., Cornell University, 1989
Office:
4-104 MCB
P: 612-624-4708

Email:
rougv001@umn.edu

 Lab:
4-220 MCB
P: 612-625-3161

Areas of Research Strength:

Gene expression
Developmental mechanisms
Genetic mechanisms

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Research Techniques:

Use of green fluorescent protein in genetic screens using
a dissecting microscope outfitted with epifluorescence

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Research Interests:

Work in the Rougvie laboratory is directed at understanding how
cells execute specific events at precise times during development.
To understand how cellular timekeeping works, the lab has chosen
to study a developmentally simply organism, the nematode
Caenorhabditis elegans. The lab is dissecting the timing mechanism
that restricts the differentiation of hypodermal cells to a time late in
the life of the worm, the transition from the larval to adult form. The
approach is to identify mutations that cause this event to occur at the
wrong time during development, and then to study the genes defined
by these mutations. These genes are referred to as ‘heterochronic’
genes because their mutation alters the relative timing and sequence
of many developmental events in the animal.

One event timed by the heterochronic genes is the terminal differentiation
of the lateral hypodermis, a process that is restricted to the final (fourth)
molt in wild-type animals and called the larval-to-adult (L/A) switch.
Mutations in heterochronic genes advance or retard the timing of the
L/A switch, resulting in larvae with adult hypodermis or adults with larval
hypodermis. We have identified several heterochronic genes through a
variety of genetic screens. For example, mutation of the gene lin-42 causes
the L/A switch to occur precociously, during the third molt. lin-42 encodes
a protein that most closely resembles the PERIOD (PER) family of proteins
from Drosophila and other organisms. This result is particularly intriguing
because PER proteins regulate circadian rhythms, a second type of biological
timing mechanism in animals: the internal clock that controls the approximately
24-hour oscillation of biological processes such as sleep-wake cycles.
Experiments are underway to investigate the similarities between LIN-42 and
PER and to understand how LIN-42 functions in the heterochronic gene pathway.
Another heterochronic gene we identified is hbl-1, the orthologue of Drosophila
hunchback. Studies of hbl-1 temporal regulation have led the lab to the study
of microRNAs, tiny, ~22 nt non-coding RNAs that down-regulate gene expression
by interacting with 3'UTRs of target genes.

The Rougvie lab will continue analysis of lin-42 and hbl-1 and its miRNA regulators,
as well as additional genes identified through ongoing genetic screens in order to
understand how the heterochronic gene pathway conveys temporal information to
cells of the developing animal. The lab's long-term goal is to determine how
developmental timing mechanisms are integrated with the spatial and sexual
cues required for proper development of a multicellular organism.


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Selected Publications:

Fukuyama, M., Rougvie, A. E., and Rothman, J. (2006) Nutrient-dependent arrest of cell cycle and growth in the C. elegans germline mediated by the DAF-18/PTEN tumor suppressor. Curr. Biol. 16, 773-779.

Tennessen, J. M., Gardner, H. F., and Rougvie, A. E. (2005). Novel heterochronic functions for the Caenorhabditis elegans period-related protein LIN-42. Dev. Biol. 289, 30-43.

Li, M., Jones-Rhoades, M. W., Lau, N. C., Bartel, D. P. and Rougvie, A. E. (2005) Regulatory mutations of mir-48, a C. elegans let-7 family microRNA, cause developmental timing defects. Dev. Cell 9, 415-422.

Rougvie, A. E. (2005). Intrinsic and extrinsic regulators of developmental timing: from miRNAs to nutritional cues. Development 132, 3787-3798.

Chan RC, chan A, Jeon M, Wu TF, Pasqualone D, Rougvie AE and Meyer BJ (2003) Chromosome cohesion is regulated by C. elegans TIM-1, a paralog of the clock protein TIMELESS. Nature, 424:1002-1009.

Abrahante, J. E., Daul, A. L., Li, M., Volk, M. L., Tennessen, J. M., Miller, E. A. and Rougvie, A. E. (2003) The Caenorhabditis elegans hunchback-like gene lin-57/hbl-1 controls developmental time and is regulated by microRNAs.  Developmental Cell 4, 625-637.

Rougvie, A. E. (2001). Control of developmental timing in animals. Nature Rev. Gen. 2, 690-701.

Reinhart, B. J., Slack, F., Basson, M., Pasquinelli, A. E., Bettinger, J., Rougvie, A. E., Horvitz, H. R. and Ruvkun, G. B. (2000). The 21 nucleotide let-7 RNA regulates developmental timing in Caenorhabditis elegans. Nature 403, 901-906.

Jeon, M., Gardner, H., Miller, E., Deshler, J. and A. E. Rougvie. (1999). The similarity of the C. elegans developmental timing protein LIN-42 with circadian rhythm proteins. Science 286, 1141-1146.

Euling, S. Bettinger, J. C., and Rougvie, A. E. (1999). The LIN-29 transcription factor is required for morphogenesis of the male tail in Caenorhabditis elegans. Dev. Biol. 206, 142-156.

Abrahante, J.E., E.A. Miller, and A.E. Rougvie. 1998. Identification of heterochronic mutants in Caenorhabditis elegans: Temporal misexpression of a collagen-green fluorescent protein fusion gene. Genetics 149: 1335-1351.

Bettinger, J.C., S. Euling, and A.E. Rougvie. 1997. The terminal differentiation factor LIN-29 is required for proper vulval morphogenesis and egg laying in Caenorhabditis elegans. Development 124: 4333-4342.

Bettinger, J.C., Lee, K. and Rougvie, A.E. 1996. Stage-specific accumulation of the terminal differentiation factor LIN-29 during Caenorhabditis elegans development. Development 122, 2517-2527.


To view these and other publications visit http://www.ncbi.nlm.nih.gov/PubMed
search menu should say PubMed
type Rougvie AE in the avaliable line

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 Last modified on Thursday, July 26, 2007