The effect of spring burning on competitive ranking of prairie species

A common explanation for the changes in species abundance following a fire is a shift in competitive ranking. However, experimental tests have been inconsistent and generally do not support this explanation. I examined the competitive ability of an abundant C 4 grass, Andropogon gerardii , and a C 3 forb, Ratibida pinnata , in a prairie remnant in northern Ohio, USA, for each of three years following a spring burn in 1996. While the abiotic environment directly influenced both species similarly, relative competitive abilities in terms of growth changed markedly: in 1996 Andropogon was less inhibited by neighbors; in 1997 both Andropogon and Ratibida had similar competitive abilities; and in 1998 Ratibida was less inhibited by neighbors. This shift in competitive response ranking paralleled the changes in relative abundance for the two species. In contrast, the effect of neighbors on survival changed markedly over time but did not differ among the two species. Thus, fire may influence species abundance through changing species competitive response ranking, at least in terms of growth.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72362/1/3236873.pd

Two new novel point mutations localized upstream and downstream of the HMG box region of the SRY gene in three Indian 46,XY females with sex reversal and gonadal tumour formation

The Y chromosome-specific gene SRY is one of the key genes involved in human sex determination. The SRY gene encodes a testis-specific transcription factor that plays a key role in sexual differentiation; development in males; is located on the distal region of the short arm of the Y chromosome. Mutations in SRY gene result in XY sex reversal; pure gonadal dysgenesis. SRY expression initiates a network of gene activity that transforms the undifferentiated gonad; genital ridge into testis. Mutations in the SRY gene have been considered to account for only 0-5% of 46;XY gonadal dysgenesis cases; whereas the majority of the remaining cases may have mutation(s) in the SRY regulatory elements or other genes involved in the sex differentiation pathway. Patients both with gonadal dysgenesis; Y-chromosome presence are at high risk of developing gonadoblastoma. Using PCR; single strand conformational polymorphism (SSCP); automated DNA sequencing; we analysed the mutations in the SRY gene in three 46;XY sex reversal patients. Two patients demonstrated nucleotide substitution (A→G) within the open reading frame just outside; upstream of the conserved DNA-binding motif called the high-mobility group (HMG) box; replacing glutamine at codon 57 with arginine. Altered SSCP patterns were also observed in these patients. Histological examination of gonads in patient revealed the formation of gonadoblastoma. Patient demonstrated A→T substitution which replaces serine at codon 4 with cysteine; just outside but downstream of the HMG box. Results suggest the involvement of SRY gene in sex reversal which further supports the relationship between SRY alterations; gonadal dysgenesis and/or primary infertility

Responses of soil cellulolytic fungal communities to elevated atmospheric CO 2 are complex and variable across five ecosystems

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/86979/1/j.1462-2920.2011.02548.x.pd

Regulation of CHK1 inhibitor resistance by a c-Rel and USP1 dependent pathway

Previously, we discovered that deletion of c-Rel in the Em-Myc mouse model of lymphoma results in earlier onset of disease, a finding that contrasted with the expected function of this NF-κB subunit in B-cell malignancies. Here we report that Em-Myc/cRel−/− cells have an unexpected and major defect in the CHK1 pathway. Total and phospho proteomic analysis revealed that Em-Myc/cRel−/− lymphomas highly resemble wild-type (WT) Em-Myc lymphomas treated with an acute dose of the CHK1 inhibitor (CHK1i) CCT244747. Further analysis demonstrated that this is a consequence of Em-Myc/cRel−/ − lymphomas having lost expression of CHK1 protein itself, an effect that also results in resistance to CCT244747 treatment in vivo. Similar down-regulation of CHK1 protein levels was also seen in CHK1i resistant U2OS osteosarcoma and Huh7 hepatocellular carcinoma cells. Further investigation revealed that the deubiquitinase USP1 regulates CHK1 proteolytic degradation and that its down-regulation in our model systems is responsible, at least in part, for these effects. We demonstrate that treating WT Em-Myc lymphoma cells with the USP1 inhibitor ML323 was highly effective at reducing tumour burden in vivo. Targeting USP1 activity may thus be an alternative therapeutic strategy in MYC-driven tumours