Single origin of human commensalism in the house sparrow.

The current, virtually worldwide distribution of the house sparrow (Passer domesticus) is a result of its commensal relationship with humans. It has been suggested that long before the advent of agriculture, an early glacial advance resulted in two disjunct ranges of ancestral house sparrows - one in the Middle East and another on the Indian subcontinent. Differentiation during this period of isolation resulted in two major groups of subspecies: the domesticus group and the indicus group. According to this hypothesis, commensalism with humans would have evolved independently in the two regions and at least twice. An alternative hypothesis is that morphological differences between the subspecies represent very recent differentiation, following expansions from a single source. To test between these hypotheses, we analysed genetic variation at the mitochondrial DNA control region and at three nuclear loci from several house sparrow populations in Europe, Asia and North Africa. No differentiation between the indicus and domesticus groups was found, supporting the single origin hypothesis. One of the subspecies in the indicus group, P. d. bactrianus, differs ecologically from other house sparrows in being migratory and in preferentially breeding in natural habitat. We suggest that bactrianus represents a relict population of the ancestral, noncommensal house sparrow. When agricultural societies developed in the Middle East about 10 000 years ago, a local house sparrow population of the bactrianus type adapted to the novel environment and eventually became a sedentary, human commensal. As agriculture and human civilizations expanded, house sparrows experienced a correlated and massive expansion in range and numbers. The pattern of genetic variation analysed here is consistent with this scenario.

Cell cycle and growth response of CHO cells to X-irradiation: threshold-free repair at low doses.

PURPOSE: To test the hypothesis of a threshold for induced repair of DNA damage (IR) and, secondarily, of hyperradiosensitivity (HRS) to low-dose X-irradiation. METHODS AND MATERIALS: Exponentially growing Chinese hamster ovary cells (CHO) were X-irradiated with doses from 0.2 to 8 Gy. Survival data were established by conventional colony-forming assay and flow-cytometric population counting. The early cell cycle response to radiation was studied based on DNA-profiles and bromodeoxyuridine pulse-labeling experiments. RESULTS: Colony-forming data were consistent with HRS. However, these data were of low statistic significance. Population counting provided highly reproducible survival curves that were in perfect accord with the linear-quadratic (LQ) model. The dominant cell cycle reaction was a dose-dependent delay of G2 M and late S-phase. CONCLUSION: There was no evidence for a threshold of IR and for low-dose HRS in X-irradiated CHO cells. It is suggested that DNA damage repair activity is constitutively expressed during S-phase and is additionally induced in a dose-dependent and threshold-free manner in late S-phase and G2. The resulting survival is precisely described by the LQ model.

Comparative analysis of apoptosis in HL60 detected by annexin-V and fluorescein-diacetate.

BACKGROUND: Our aim was to compare and evaluate apoptosis formation as detected by propidium-iodide (PI)/annexin-V or PI/fluorescein-diacetate (FDA) as dose-response parameters in a human promyelocytic leukemia cell line, HL60. METHODS: In exponentially growing HL60 cells, apoptosis was induced by ionizing radiation, hyperthermia, topotecan, and cytosine beta-D-arabinofuranoside. At 4 consecutive days following induction, apoptosis was detected by double-labelling, either with PI/annexin-V or PI/FDA. Forward and side scatter, red (PI), and green (FDA or annexin-V) fluorescence were measured by flow cytometry. RESULTS: While light scatter discriminated between morphologically damaged and undamaged cells, fluorescence differentiated vital, apoptotic, and dead cells. Equal proportions of these three subpopulations were detected by both staining techniques. Occasionally, early and mature apoptoses were identified as distinct clusters. During the 4-day observation period, no pronounced maxima of the apoptotic fractions were obtained with either treatment modality. The gradual increases usually showed a delay of 1-2 days. CONCLUSIONS: FDA and annexin-V are equally suitable for detecting apoptosis. Separation improves with time after induction, indicating that, with respect to test specificity, mature apoptoses are superior to early stages. However, the sensitivity towards low rates of apoptosis after weak induction appears limited with both staining procedures.