First name,Last name,Preferred title,Overview,Position,Department,Individual
Bruce,Riley,Professor,"My lab studies inner ear development in zebrafish. A prominent feature of our research is to investigate how cell-cell signaling and downstream gene-interactions control development. One project in the lab focuses on how cell signaling regulates ectodermal patterning during gastrulation to establish the otic placode, the precursor of the inner ear. Our recent work shows that localized Fgf signaling is especially critical for inducing formation of the otic placode, and members of the Pax2/5/8 family of transcription factors are important mediators of Fgf signaling. During later stages of inner ear development, we are exploring how sensory hair cells and neurons are regulated. Our studies address how these cells initially form, how they are genetically maintained, and how they become specialized for hearing vs. balance. We are also investigating how zebrafish can replace dead and damaged hair cells, an ability that mammals have lost. The inability to regenerate hair cells explains why humans show progressive irreversible hearing loss as we age. It is hoped that activating or augmenting human homologs of genes shown to operate in zebrafish might help restore hearing and balance in humans.",Professor,Biology,https://scholars.library.tamu.edu/vivo/display/n0dbb8253
Benjamin,Neuman,Professor,,Professor,Biology,https://scholars.library.tamu.edu/vivo/display/n193ea580
Deborah,Bell-Pedersen,Professor,"Research in the Bell-Pedersen lab focuses on determining how the circadian clock functions in organisms to regulate daily rhythms in gene expression, behavior, and physiology. The molecular clock in higher eukaryotes involves a master clock in the brain regulating clocks in peripheral tissues, posing significant obstacles for understanding circadian output mechanisms. Thus, a major strength of our work is using a single-celled model eukaryote, Neurospora crassa, to elucidate the underlying mechanisms of rhythmic gene expression and protein synthesis. Clock dysfunction in humans is associated with a wide range of diseases, including cardiovascular disease, cancer, metabolic disorders, mental illness, sleep disorders, and aging. In addition, daily changes in metabolism and cell division rates influence the efficacy and toxicity of many pharmaceuticals, including cancer drugs. Therefore, knowing how clocks work to control rhythmic gene expression, and what they regulate, is critical for the development of therapeutics. Research to understand clock-controlled rhythmic gene expression has focused primarily on transcriptional mechanisms, and little was known about posttranscriptional control. We discovered that the clock regulates highly conserved translation initiation and elongation factors, tRNA synthetase levels, and ribosome heterogeneity. This regulation determines what mRNAs are rhythmically translated and the accuracy of the translation process (translation fidelity). We are capitalizing on these exciting discoveries to determine how the clock regulates translation fidelity. These studies will provide the foundation for understanding the impact of daily rhythms in translation fidelity on protein diversity beyond what is encoded for in the genome.",Professor and Associate Department Head,Biology,https://scholars.library.tamu.edu/vivo/display/n2a2bfb97
Christine,Merlin,Associate Professor,"Our research broadly lies in understanding how organisms respond and adapt to changing environments, with an emphasis on circadian biology. Organisms from bacteria to humans use circadian clocks to control a plethora of biochemical, physiological and behavioral rhythms. These clocks are synchronized to daily and seasonal environmental changes to allow organisms to tune specific activities at the appropriate times of day or year.
In our laboratory, we use the eastern North American migratory monarch butterfly (Danaus plexippus) as a model system to study animal clock mechanisms and the role of circadian clocks and clock genes in a fascinating biological output, the animal long-distance migration. Every fall, like clockwork, millions of monarch butterflies start migrating thousands of miles from North America to reach their overwintering sites in central Mexico. During their journey south, migrating monarchs use a time-compensated sun compass orientation mechanism to maintain a constant flight bearing. Circadian clocks located in the antennae provide the critical internal timing device for compensation of the sun movement across the sky over the course of the day. The recent sequencing of the monarch genome and the establishment of genetic tools to knockout clock genes (and others) in vivo using nuclease-mediated gene targeting approaches provides us with a unique opportunity to uncover the molecular and cellular underpinnings of the butterfly clockwork, its migratory behavior and their interplay.",Assistant Professor,Biology,https://scholars.library.tamu.edu/vivo/display/n5a23a5d7
Heath,Blackmon,Associate Professor,,Assistant Professor||Associate Professor,Biology||Biology,https://scholars.library.tamu.edu/vivo/display/n6e56235d
Paul,Hardin,Distinguished Professor,"A diverse array of organisms including prokaryotic and eukaryotic microbes, plants, and animals display daily rhythms in physiology, metabolism and/or behavior. These rhythms are not passively driven by environmental cycles of light and temperature, but are actively controlled by endogenous circadian clocks that are set by environmental cycles, keep time in the absence of environmental cues, and activate overt physiological, metabolic and behavioral rhythms at the appropriate time of day. This remarkable conservation of circadian clock function through evolution suggests that maintaining synchrony with the environment is of fundamental importance. Our understanding of the circadian clock is particularly important for human health and well-being. The clearest examples of circadian clock dysfunction are those that result in abnormal sleep-wake cycles, but clock disturbances are also associated with other ailments including epilepsy, cerebrovascular disease, depression, and seasonal affective disorder. The realization that disorders of the sleep-wake cycle such as Familial Advanced Sleep Phase Syndrome can result from alterations in clock gene function underscores the clinical importance of understanding the molecular organization of the circadian system.
Work in my laboratory focuses on defining the molecular mechanisms that drive circadian clock function in the fruit fly, Drosophila melanogaster. We previously found that the core timekeeping mechanism is based on core and interlocked transcriptional feedback loops. Our studies currently focus on (1) defining post-translational regulatory mechanisms that operate in the core loop to set the 24 hour period, (2) determining whether interlocked loops are important for circadian timekeeping and/or output, (3) understanding how circadian oscillator cells are determined during development, and (4) defining mechanisms that control rhythms in olfactory and gustatory physiology and behavior.",Distinguished Professor,Biology,https://scholars.library.tamu.edu/vivo/display/nf27056c4
Richard,Gomer,Distinguished Professor,"Our laboratory is working on three areas of biomedicine, trying to move observations from basic research into the clinic. First, we are studying how the sizes of tissues and tumors are regulated, and how this can be manipulated for therapeutic purposes. As a model system, we are using the simple eukaryote Dictyostelium discoideum, which allows us to combine techniques such as biochemistry, genetics, computer modeling, and cell biology to study tissue size regulation. We have found that a secreted protein as well as the unusual molecule polyphosphate are signals in negative feedback loops that inhibit Dictyostelium cell proliferation, and we are studying the signal transduction pathway to understand similar mechanisms in humans.
Second, we are studying how some secreted proteins can make cells move away from the source of the signal. We found such a signal (called a chemorepellent) in Dictyostelium, and then found a similar signal in humans. We are working to understand the signal transduction pathway for both. The human signal repels neutrophils, and we found that this can be used therapeutically in mouse models of neutrophil-driven diseases such as rheumatoid arthritis and acute respiratory distress syndrome.
Third, we have found that a human blood protein called Serum Amyloid P (SAP) regulates a key step in the formation of scar tissue as well as the formation of the scar-like lesions in fibrosing diseases such as congestive heart failure and pulmonary fibrosis. We are studying this mechanism, and a biotech company (Promedior, now sold to Roche) we co-founded is testing SAP as a therapy for fibrosis in patients in a Phase 3 trials.",Distinguished Professor,Biology,https://scholars.library.tamu.edu/vivo/display/nf41f3898
Uel,Mcmahan,Professor,"McMahan and his research group provide one of the cornerstones for Texas A&M's new Interdisciplinary Life Sciences Building and its related teaching and research efforts. His work focuses on how the nervous system's synapses form in the embryo and function in the adult in various animal species. It relies on high-resolution imaging, chemical characterization and experimental manipulation of specific macromolecules and organelles, which altogether provide insights unobtainable via any other approach. The findings bear directly on the problems of understanding the molecular basis of human brain diseases and restoring brain function after trauma.",Professor,Biology,https://scholars.library.tamu.edu/vivo/display/nfc3672e7