Meteoroid Fragmentation in the Martian Atmosphere and the Formation of Crater Clusters.

The current rate of small impacts on Mars is informed by more than one thousand impact sites formed in the last 20 years, detected in images of the martian surface. More than half of these impacts produced a cluster of small craters formed by fragmentation of the meteoroid in the martian atmosphere. The spatial distributions, number and sizes of craters in these clusters provide valuable constraints on the properties of the impacting meteoroid population as well as the meteoroid fragmentation process. In this paper, we use a recently compiled database of crater cluster observations to calibrate a model of meteoroid fragmentation in Mars' atmosphere and constrain key model parameters, including the lift coefficient and fragment separation velocity, as well as meteoroid property distributions. The model distribution of dynamic meteoroid strength that produces the best match to observations has a minimum strength of 10-90 kPa, a maximum strength of 3-6 MPa and a median strength of 0.2-0.5 MPa. An important feature of the model is that individual fragmentation events are able to produce fragments with a wide range of dynamic strengths as much as 10 times stronger or weaker than the parent fragment. The calibrated model suggests that the rate of small impacts on Mars is 1.5-4 times higher than recent observation-based estimates. It also shows how impactor properties relevant to seismic wave generation, such as the total impact momentum, can be inferred from cluster characteristics.

The catalytic subunit alpha' gene of human protein kinase CK2 (CSNK2A2): genomic organization, promoter identification and determination of Ets1 as a key regulator.

The human genome contains four protein kinase CK2 loci, enclosing three active genes coding for the catalytic subunits alpha and alpha' and the regulatory subunit beta, and a processed alpha subunit pseudogene. Extensive structure and transcriptional control data of the genes are available, except for the CK2alpha' gene (CSNK2A2). Using in silico and experimental approaches, we find CSNK2A2 to be located on the long arm of chromosome 16 (in contrast to published data), to span 40kb and to consist of 12 exons, with the translational start in Exon 1 and the stop in Exon 11. Exon/intron boundaries conform to the gt/ag rule, and various potential polyadenylation signals determine transcript species with lengths of 1.7-5.7 kb. The upstream region of the gene displays housekeeping characteristics, lacking a TATA box and possessing several GC boxes as well as a CpG island around Exon 1. According to reporter gene assay results, the promoter activity ranges from -1308 to 197 with the highest activity in region -396 to -129. This region contains binding motifs for various transcription factors, including NFkappaB, Sp and Ets family members. Site-directed mutagenesis indicates that the Ets motifs play, in cooperation with Sp motif clusters, a central role in regulating CK2alpha' gene transcription. A similar control has been described for the transcription of the CK2alpha and CK2beta genes so that the presented data are compatible with the assumption of a coordinate transcriptional regulation of all three active human CK2 genes decisively determined by Ets family members.

Bone metastasis: Osteoblasts affect growth and adhesion regulons in prostate tumor cells and provoke osteomimicry.

Bone metastasis is the primary cause of death in human prostate cancer. Disseminated from primary tumor and distributed via the bloodstream, a proportion of prostate carcinoma cells eventually reach the skeleton and develop into metastases, requiring adhesion to inner bone surfaces lined by osteoblasts. The crosstalk of tumor cells with osteoblasts is a critical but poorly characterized step in the metastatic process. Using an in vitro metastasis model system, we have been examining effects of osteoblast-released factors on gene expression of prostate carcinoma cells. Here, we show by large-scale transcript profiling and quantitative RT-PCR that osteoblast-released factors target in particular the proliferation and adhesion regulons of tumor cells. Genes encoding components of the cell-cycle control machinery and connected pathways are predominantly repressed and cell proliferation is slowed down, resembling in vivo observations assumed to render commonly used chemotherapeutic measures ineffective. Genes encoding anchoring junction components are predominantly elevated, and the adhesion properties of tumor cells are altered. Moreover, prostate carcinoma cells are provoked to undergo osteomimicry, i.e., to express bone cell-related genes. The data indicate that the crosstalk with osteoblasts induces expressional changes in prostate carcinoma cells favoring the bone colonization process.