Abstract. A 39-winter (1963-2001) record of annual maximum ice concentration (AMIC), the maximum fraction of lake surface area covered by ice each year, is analyzed for each Great Lake. Lake Erie has the largest median AMIC (94%) followed by Lakes Superior (80%), Huron (63%), Michigan (33%), and Ontario (21%). The frequency distribution of AMICs is negatively skewed for Lakes Superior and Erie and positively skewed for Lakes Michigan and Ontario. Temporal and spatial patterns of typical and extreme AMICs is presented within the context of long-term average air temperatures and lake bathymetry. The variation of spatially averaged ice concentration with discrete depth ranges are discussed for each lake for the upper and lower end of the typical range of AMIC values. In general, ice concentration decreases with increasing depth ranges for a given winter. A decrease in the gradient of ice concentration with depths was also observed with an increase in the AMIC from winter 1983 to winter 1984. A temporal trend in the AMICs supports the hypothesis of three ice cover regimes over the past 39 winters. Approximately 44% of the highest quartile (10 highest) AMICs for the Great Lakes occurred during the 6-winter period: 1977-1982 providing evidence of a higher ice cover regime during this period relative to the 14 winters before them (1963)(1964)(1965)(1966)(1967)(1968)(1969)(1970)(1971)(1972)(1973)(1974)(1975)(1976) and the 19 winters after them (1983)(1984)(1985)(1986)(1987)(1988)(1989)(1990)(1991)(1992)(1993)(1994)(1995)(1996)(1997)(1998)(1999)(2000)(2001). Winter 1998 established new low AMIC extremes, and the AMIC averaged over the 1998-2001 winters is the lowest for the period of record on four of the five Great Lakes. These recent trends taken together are noteworthy as they may be harbingers of a period of even lower AMICs in the 21st Century.
The T-box gene Eomesodermin (Eomes) is required for early embryonic mesoderm differentiation in mouse, frog (Xenopus laevis), and zebrafish, is important in late cardiac development in Xenopus, and for CD8؉ T effector cell function in mouse. Eomes can ectopically activate many mesodermal genes. However, the mechanism by which Eomes activates transcription of these genes is poorly understood. We report that Eomes protein interacts with Smad2 and is capable of working in a non-cell autonomous manner via transfer of Eomes protein between adjacent embryonic cells. Blocking of Eomes protein transfer using a farnesylated red fluorescent protein (CherryF) also prevents Eomes nuclear accumulation. Transfer of Eomes protein between cells is mediated by the Eomes carboxyl terminus (456 -692). A carbohydrate binding domain within the Eomes carboxyl-terminal region is sufficient for transfer and important for gene activation. We propose a novel mechanism by which Eomes helps effect a cellular response to a morphogen gradient.
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