Todd Lamitina, Ph.D.
Assistant Professor, Department of Physiology

Cell Biology and Physiology

Address

A700 Richards Research Bldg.
3700 Hamilton Walk
Philadelphia, PA 19104
Office tel.: 215-898-3223
Lab tel.: 215-898-0566
E-mail: lamitina@mail.med.upenn.edu


Education

Emory University: BS (Biology), 1995.

Emory University: PhD (Cell and Developmental Biology), 2002.

Links:
Lamitina Lab

Research Interests

• Molecular mechanisms of environmental stress sensing and signaling

Key words: Osmoregulation, protein damage, salt and water balance, environmental stress, C. elegans, genomics

Search PubMed for articles

Description of Research

The ability to detect and repair cellular and molecular damage induced by environmental stress is essential for all forms of life. Stress-induced damage can arise from normal physiological processes, such as urinary concentration in the kidney or ageing, as well as numerous disease states, including Alzheimer’s, Parkinson’s, diabetes, and renal failure. A better understanding of these damage control mechanisms could have important consequences for understanding and treating these diseases. While genetic approaches have been used with much success to understand environmental stress signaling in plants, bacteria, and yeast, similar approaches have not been applied to animals.

The nematode C. elegans offers significant experimental advantages for defining the molecular bases of environmental stress signaling. In the Lamitina lab, we use high-throughput forward and reverse genetic screening, transgenics, in vivo imaging, microarrays, quantitative physiological assays, and integrative computational tools to define the sensing and signaling mechanisms underlying the response to environmental stressors. Our current efforts are focused on deciphering the response to osmotic stress, which is essential for all forms of cellular life and plays a particularly important role in renal physiology. From a genome-wide RNAi screen, we have discovered that protein damage, which is a well known consequence of osmotic stress, functions as a signal to specifically active the gene expression program underlying the response to osmotic stress. Our short term goals are to 1) utilize genetic and genomic approaches in C. elegans to define the molecules that directly sense osmotically induced protein damage 2) explore the signal transduction pathways that mediate changes in osmosensitive gene expression, and 3) understand the large-scale systems logic that underlies the response to environmental stress, using the osmotic stress response as a model.

Recent Publications

ALamitina T, Huang CG and Strange K. Genome-wide RNAi screening identifies protein damage as a regulator of osmoprotective gene expression. Proc Natl Acad Sci U S A 103: 12173-12178, 2006.

Lamitina T. Functional Genomic Approaches in C. elegans. Methods Mol Biol 351: 127-138, 2006.

Yan X, Xing J, Lorin-Nebel C, Estevez AY, Nehrke K, Lamitina T and Strange K. Function of a STIM1 Homologue in C. elegans: Evidence that Store-operated Ca2+ Entry Is Not Essential for Oscillatory Ca2+ Signaling and ER Ca2+ Homeostasis. J Gen Physiol 2006.

Huang CG, Agre P, Strange K and Lamitina T. Isolation of C. elegans Deletion Mutants Following ENU Mutagenesis and Thermostable Restriction Enzyme PCR Screening. Mol Biotechnol 32: 83-86, 2006.

Lamitina ST, Morrison R, Moeckel GW and Strange K. Adaptation of the nematode Caenorhabditis elegans to extreme osmotic stress. Am J Physiol Cell Physiol 286: C785-C791, 2004.

Lab

Rotation Projects for 2006-2007

• Identify transcription factors that regulate osmosensitive gene expression
• Characterize the role of a novel kinase in the regulation of osmosensitive gene expression and other stress responses
• Define the gene expression programs associated with osmotic stress
• Establish a C. elegans model for defining regulators of heat shock transcription factor 1

Lab personnel:

Yana Miteva - Research Technician