Control of distal antennal identity and tarsal development in Drosophila by spineless-aristapedia, a homolog of the mammalian dioxin receptor.

We report the molecular characterization of the spineless (ss) gene of Drosophila, and present evidence that it plays a central role in defining the distal regions of both the antenna and leg. ss encodes the closest known homolog of the mammalian dioxin receptor, a transcription factor of the bHLH-PAS family. Loss-of-function alleles of ss cause three major phenotypes: transformation of distal antenna to leg, deletion of distal leg (tarsal) structures, and reduction in size of most bristles. Consistent with these phenotypes, ss is expressed in the distal portion of the antennal imaginal disc, the tarsal region of each leg disc, and in bristle precursor cells. Ectopic expression of ss causes transformation of the maxillary palp and distal leg to distal antenna, and induces formation of an ectopic antenna in the rostral membrane. These effects indicate that ss plays a primary role in specifying distal antennal identity. In the tarsus, ss is expressed only early, and is required for later expression of the tarsal gene bric à brac (bab). Ectopic expression causes the deletion of medial leg structures, suggesting that ss plays an instructive role in the establishment of the tarsal primordium. In both the antenna and leg, ss expression is shown to depend on Distal-less (Dll), a master regulator of ventral appendage formation. The antennal transformation and tarsal deletions caused by ss loss-of-function mutations are probably atavistic, suggesting that ss played a central role in the evolution of distal structures in arthropod limbs.

Dietary fats and colon cancer: assessment of risk associated with specific fatty acids.

There are many biological mechanisms whereby dietary fat and specific dietary fatty acids may alter risk of colon cancer in addition to their contribution to total energy intake. To evaluate these potential associations, we used detailed dietary intake data collected in a population-based study of 1,993 incident colon cancer cases and 2,410 controls conducted in 3 areas of the United States. The most commonly consumed fatty acid in the study population was oleic acid. One-third of dietary fats consumed came from additions to other foods at the table or from the preparation of other foods. After adjusting for total energy intake, physical activity and body size, neither total dietary fat nor specific fatty acids was associated with risk of colon cancer. However, among older women, fats from food preparation were associated with increased risk of colon cancer (OR 1.84, 95% CI 1.20-2.80), while fats from foods themselves or from additions to other foods were not. While dietary fats were not associated with colon cancer risk in the total population, subgroups of the population appeared to be at slightly greater risk if they consumed a high-fat diet. Women who consumed a diet high in mono-unsaturated fatty acids (MFAs) and poly-unsaturated fatty acids (PFAs) and who had a family history of colorectal cancer were at greater risk of colon cancer than those with similar intakes but without a family history of colorectal cancer. Similar associations with family history were noted among men diagnosed at younger ages for MFA, linolenic acid and 20-carbon PFA.

Plant foods and colon cancer: an assessment of specific foods and their related nutrients (United States).

Plant foods have been associated inversely with colon cancer. Since a major focus of this study was to identify components of plant foods which may account for their association with colon cancer, nutrients which are commonly found in plant foods also were evaluated. A population-based case-control study was conducted in Northern California, Utah, and the 'Twin Cities' area of Minnesota (United States). Complete data were available from interviewer-administered questionnaires on 1,993 cases and 2,410 controls. Higher intakes of vegetables (for highest relative to lowest quintile of intake) were associated inversely with colon cancer risk: the odds ratio (OR) was 0.7 for both men (95 percent [CI] confidence interval = 0.5-0.9) and women (CI = 0.5-1.0). Associations were stronger among those with proximal tumors. Total fruit intake was not associated with colon cancer risk although, among men, higher levels of whole grain intake were associated with a decreased risk (OR = 0.6, CI = 0.4-0.9 for older men); high intakes of refined grains were associated with an increased risk (OR = 1.5, CI = 1.1-2.1). Dietary fiber intake was associated with a decreased risk of colon cancer: OR = 0.5 (CI = 0.3-0.9) for older men; OR = 0.7 (CI = 0.4-1.2) for older women; OR = 0.6 (CI = 0.4-1.0) for men with proximal tumors; OR = 0.5 (CI = 0.3-0.9) for women with proximal tumors. Other nutrients, for which plant foods were the major contributor--such as vitamin B6, thiamin, and niacin (women only)--also were associated inversely with colon cancer. Neither beta-carotene nor vitamin C was protective for colon cancer. Adjustment of plant foods for nutrients found in plant foods or for supplement use did not appreciably alter the observed associations between plant foods and colon cancer.