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The quantification of rates for the competing forces of tectonic uplift and erosion has important implications for understanding topographic evolution. Here, we quantify the complex interplay between tectonic uplift, topographic development, and erosion recorded in the hanging walls of several active reverse faults in the Ventura basin, southern California, USA. We use cosmogenic 26Al/10Be isochron burial dating and 10Be surface exposure dating to construct a basin-wide geochronology, which includes burial dating of the Saugus Formation: an important, but poorly dated, regional Quaternary strain marker. Our ages for the top of the exposed Saugus Formation range from 0.36 +0.18/-0.22 Ma to 1.06 +0.23/-0.26 Ma, and our burial ages near the base of shallow marine deposits, which underlie the Saugus Formation, increase eastward from 0.60 +0.05/-0.06 Ma to 3.30 +0.30/-0.41 Ma. Our geochronology is used to calculate rapid long-term reverse fault slip rates of 8.6-12.6 mm yr-1 since ca. 1.0 Ma for the San Cayetano fault and 1.3-3.0 mm yr-1 since ca. 1.0 Ma for the Oak Ridge fault, which are both broadly consistent with contemporary reverse slip rates derived from mechanical models driven by global positioning system (GPS) data. We also calculate terrestrial cosmogenic nuclide (TCN)-derived, catchment-averaged erosion rates that range from 0.05-1.14 mm yr-1 and discuss the applicability of TCN-derived, catchment-averaged erosion rates in rapidly uplifting, landslide-prone landscapes. We compare patterns in erosion rates and tectonic rates to fluvial response times and geomorphic landscape parameters to show that in young, rapidly uplifting mountain belts, catchments may attain a quasi-steady-state on timescales of <105 years even if catchmentaveraged erosion rates are still adjusting to tectonic forcing. [ABSTRACT FROM AUTHOR]

Intrathymic injection of the Abelson murine leukemia virus (A-MuLV) results in transformation of immature T and B lymphoid cells. In this report we demonstrate that the concentration of A-MuLV injected into murine thymi influences the selection of the transformation target. Thus, concentrated A-MuLV gives rise to Thy-1+ B220- thymomas. In contrast, dilute virus induces B220+ thymomas that also express low levels of Thy-1 (Thy-1lo), a phenotype that is similar to marrow-derived progenitor B-lymphoid cells (pro-B cells) that are highly susceptible to A-MuLV transformation in vitro. However, rare B220+ lymphoid cells isolated from normal adult thymi were not transformed by A-MuLV in vitro, while B220+ cells isolated from bone marrow were highly susceptible to transformation by A-MuLV. The Thy-1lo B220+ population in the primary thymomas had not rearranged TCRgamma, TCRbeta, or Igkappa genes, but contained subpopulations that assembled Ig DJ(H) or VDJ(H) genes and were therefore similar to transformed pro- and pre-B cells obtained from A-MuLV infected fetal liver and adult bone marrow, respectively. However, unlike A-MuLV-transformed pro- and pre-B cells, many (40-70%) of the Thy-1lo B220+ transformed thymoma cells had not rearranged Igh genes, and therefore appear to represent undifferentiated lymphoid cells. We conclude that A-MuLV may transform an undifferentiated lymphoid target in the thymus.

We have developed an in vitro gene trap screen for novel murine genes that allows one to determine, prior to making chimeric or transgenic animals, if these genes are expressed in one or more specific embryonic tissues. Totipotent embryonic stem (ES) cells are infected with a retroviral gene trap construct encoding a selectable lacZ/neo fusion gene, which is expressed only if the gene trap inserts within an active transcription unit. G418-resistant ES cell clones are induced to differentiate in vitro, and neurons, glia, myocytes, and chondrocytes are screened for expression of beta-galactosidase (beta-gal). cDNAs of the gene trap transcripts are obtained by 5' rapid amplification of cDNA ends and are sequenced to determine if they represent novel genes. In situ hybridization analyses show that trapped genes are expressed in vivo within the cell types that express beta-gal in vitro. Gene traps and their wild-type alleles are characterized in terms of copy number, alternate splicing of their transcripts, and the proportion of endogenous mRNA sequence that is replaced by lacZ/neo in the hybrid gene trap transcript. This approach, which we term "in vitro preselection," is more economical than standard in vivo gene trap screening because tissue-specific expression of probable knockout alleles is verified before transgenic animals are generated. These results also highlight the utility of ES cell differentiation in vitro as a method with which to study the molecular mechanisms regulating the specification and commitment of a variety of cell and tissue types.

Basic helix-loop-helix (bHLH) proteins often belong to a family of transcription factors that bind to the DNA target sequence -CANNTG- (E-box) that is present in the promoter or enhancer regions of numerous developmentally regulated genes. In this study, we report the isolation and initial characterization of a novel bHLH factor, termed Mist1, that was identified by virtue of its ability to interact with E-box regulatory elements in a yeast "one-hybrid" screening procedure. Northern analysis revealed that Mist1 transcripts are expressed in several adult tissues, including stomach, liver, lung, and spleen but no expression is detected in the heart, brain, kidney, or testis. During mouse embryogenesis, Mist1 mRNA is first observed at E10.5 in the primitive gut and in the developing lung bud. Expression persists through E16.5 and remains restricted primarily to the epithelial lining. Mist1 also is detected in skeletal muscle tissues beginning at E12.5, persisting throughout all embryonic stages examined although in older embryos and in the adult expression becomes severely reduced. At later developmental times, Mist1 transcripts also are found in the pancreas, submandibular gland, and adult spleen. As predicted, the Mist1 protein is nuclear and binds efficiently to E-box sites as a homodimer. Mist1 also is capable of binding to E-box elements when complexed as a heterodimer with the widely expressed E-proteins, E12 and E47. Surprisingly, although Mist1 binds to E-boxes in vivo, the Mist1 protein lacks a functional transcription activation domain. These observations suggest that Mist1 may function as a unique regulator of gene expression in several different embryonic and postnatal cell lineages.