Telomerase reverse transcriptase (TERT) promotes the expression of the enzyme telomerase, which is responsible for copying the ends of chromosomes known as telomeres. Maintaining telomere length is necessary for the growth, survival, and injury prevention of cells. But, after birth, TERT production normally stops in most cell types. Consequently, telomeres are incapable of unlimited proliferation as they shorten during the aging process. Researchers at the Baylor College of Medicine, Waco, Texas, have engineered mice to produce TERT at levels found only in embryonic cells (O. Hidemasa et al., "Telomerase reverse transcriptase promotes cardiac muscle cell proliferation, hypertrophy, and survival," Proceedings of the National Academy of Sciences, 98[18], 10308-13, Aug. 28, 2001.) Forcing TERT expression in the mice showed a reduced loss of telomerase activity in postmitotic myocardium, maintenance of telomere length, and delay in cardiac cell exit. After proliferation ceased, hypertrophy (cell enlargement) took place. But, hypertrophy's normal adverse conditions, fibrosis and cell death, did not occur. Lead researcher Michael D. Schneider comments, "Typically, hypertrophy causes myocytes to become meshed in fibrotic tissues, making it stiff and unable to contract as well. Here, we observed not only an increase in cardiac mass but with normal contraction as well." The elevated levels of telomerase from TERT production reduced the size of the heart attacks and subsequent heart damage. Schneider predicts that these findings could lead to new heart treatments, including engineered, graftable TERT cells and gene therapy treatment delivering TERT to the heart.
Linking Auxin to Plants' Light-Response Pathways
It's been known since the late 1920s that changes in the level of the plant hormone, auxin, occur during light-induced responses. Researchers at the Salk Institute for Biological Studies in La Jolla, Calif., have recently found genetic evidence linking auxin to the light-response pathways in plants. (J. Chory et al., "BIG: a calossin-like protein required for polar auxin transport in Arabidopsis," Genes and Development, 15[15], 1985-97, Aug. 1, 2001). The research centers around two mutants, exhibiting different properties, which were identified in separate screens. The mutant doc1 was known to misexpress its light-regulated genes by functioning in the dark. The tir3 mutant was known to resist auxin transport inhibitors. However, researchers found that a genetic cross of the mutants showed that these two strains harbor mutations in the same gene, dubbed BIG, as a tribute to its enormous size, which is 560 kilodaltons. BIG is thought to encode a large protein that has a similar identity to the Drosophila protein calossin, found to be involved in photoreceptor-signaling in eyes, and is essential in altering auxin signaling and transport. Principal investigator Joanne Chory notes, "Because BIG helps auxin and membrane proteins get to where they need to be, it will link a basic cellular process with an important developmental response." A number of additional mutations affecting auxin physiology and photomorphogenesis were also isolated from the gene. Chory seems optimistic about the possible implications of this finding: "It's important to find what other proteins BIG interacts with and how they are being expressed in a cell. A protein like this may be involved in linking a lot of pathways to cell expansion."
