Biological correlates of extinction risk in bats

We investigated patterns and processes of extinction and threat in bats using a multivariate phylogenetic comparative approach. Of nearly 1,000 species worldwide, 239 are considered threatened by the International Union for Conservation of Nature and Natural Resources (IUCN) and 12 are extinct. Small geographic ranges and low wing aspect ratios are independently found to predict extinction risk in bats, which explains 48% of the total variance in IUCN assessments of threat. The pattern and correlates of extinction risk in the two bat suborders are significantly different. A higher proportion (4%) of megachiropteran species have gone extinct in the last 500 years than microchiropteran bats (0.3%), and a higher proportion is currently at risk of extinction (Megachiroptera: 34%; Microchiroptera: 22%). While correlates of microchiropteran extinction risk are the same as in the order as a whole, megachiropteran extinction is correlated more with reproductive rate and less with wing morphology. Bat extinction risk is not randomly distributed phylogenetically: closely related species have more similar levels of threat than would be expected if extinction risk were random. Given the unbalanced nature of the evolutionary diversification of bats, it is probable that the amount of phylogenetic diversity lost if currently threatened taxa disappear may be greater than in other clades with numerically more threatened species.     

Maintenance of the inner cell mass in human blastocysts from fragmented embryos

The degree of fragmentation during early cleavage is universally used as an indicator of embryo quality during human in vitro fertilization treatment. Extensive fragmentation has been associated with reduced blastocyst formation and implantation. We examined the relationship between early fragmentation and subsequent allocation of cells to the trophectoderm and inner cell mass in the human blastocyst. We retrospectively analyzed data from 363 monospermic human embryos that exhibited varying degrees of fragmentation on Day 2. Embryos were cultured from Day 2 to Day 6 in Earle balanced salt solution with 1 mM glucose and human serum albumin. Rates of development and blastocyst formation were measured. The number of cells in the trophectoderm and inner cell mass and the incidence of apoptosis were assessed following differential labeling with polynucleotide-specific fluorochromes. Increasing fragmentation resulted in reduced blastocyst formation and lower blastocyst cell numbers. For minimal and moderate levels of fragmentation, the reduction in cell numbers was confined largely to the trophectoderm and a steady number of inner cell mass cells was maintained. However, with extensive fragmentation of more than 25%, cell numbers in both lineages were reduced in the few embryos that formed blastocysts. Apoptotic nuclei were present in both the trophectoderm and inner cell mass, with the lowest incidence in blastocysts that had developed from embryos with minor (5-10%) fragmentation. Paradoxically, higher levels of apoptosis were seen in embryos of excellent morphology, suggesting a possible role in regulation of cell number.     

Evidence for a second gene for primary microcephaly at MCPH5 on chromosome 1

Primary microcephaly has been mapped to five loci on different chromosomes. We present here the fine mapping of one of the loci, MCPH5, to a region of only 0.58 Mb located at the 1q31.3-1q32.1 junction. A genome scan was performed on five families from the Netherlands and Jordania, with 14 patients affected by microcephaly. A maximum LOD score of 4.78 was found for marker D1S1660 at the MCPH5 locus. Haplotype analysis suggests that the gene causing microcephaly is located between markers D1S3469 and D1S1660, which excludes the previously reported ASPM gene.     

Repeated inoculation as a strategy for the remediation of low concentrations of phenanthrene in soil

Phenanthrene, a polycyclic aromatic hydrocarbon, becomes increasingly unavailable to microorganisms for degradation as it ages in soil. Consequently, many bioaugmentation efforts to remediate polycyclic aromatic hydrocarbons in soil have failed. We studied theeffect of repeatedly inoculating a soil with a phenanthrene-degrading Arthrobacter sp. on the mineralization kinetics of low concentrations of phenanthrene. After the first inoculation, the initial mineralization rate of 50 ng/g phenanthrene declined in a biphasicexponential pattern. By three hundred hours after inoculation, there was no difference in mineralization rates between the inoculated and uninoculated treatments even though a large fraction of the phenanthrene had not yet been mineralized. A second and third inoculation significantly increased the mineralization rate, suggesting that, though themineralization rate declined, phenanthrene remained bioavailable. Restirring the soil, without inoculation, did not produce similar increases in mineralization rates, suggesting absence of contact between cells and phenanthrene on a larger spatial scale (>mm) is not the cause of the mineralization decline. Bacteria inoculated into soil 280 hours beforethe phenanthrene was added could not maintain phenanthrene degradation activity. We suggest sorption lowered bioavailability of phenanthrene below an induction threshold concentration for metabolic activity of phenanthrene-degrading bacteria.     

CD8 T cells are sufficient to mediate allorecognition and allograft rejection

Different T cell subsets may play different roles in allorecognition and allograft rejection. It has been suggested that CD8 T cells can only initiate rejection with help from CD4 T cells. Since CD8 T cells may have different requirements for allorecognition and for costimulation, it is important to clarify the role of CD8 cells in rejection. We examined the role of CD8 cells in allorecognition using a TCR transgenic mouse transplantation model. In our study, CD8 cells were able to recognize alloantigens and reject allografts in the absence of help from CD4 T cells. Furthermore our study provides a model to study the mechanisms of CD8-mediated allograft rejection. It may be important in the future, to consider that CD8 T cells may need to be targeted independently of CD4 T cells in strategies used to prevent rejection and induce tolerance.     

FQR1, a novel primary auxin-response gene, encodes a flavin mononucleotide-binding quinone reductase

FQR1 is a novel primary auxin-response gene that codes for a flavin mononucleotide-binding flavodoxin-like quinone reductase. Accumulation of FQR1 mRNA begins within 10 min of indole-3-acetic acid application and reaches a maximum of approximately 10-fold induction 30 min after treatment. This increase in FQR1 mRNA abundance is not diminished by the protein synthesis inhibitor cycloheximide, demonstrating that FQR1 is a primary auxin-response gene. Sequence analysis reveals that FQR1 belongs to a family of flavin mononucleotide-binding quinone reductases. Partially purified His-tagged FQR1 isolated from Escherichia coli catalyzes the transfer of electrons from NADH and NADPH to several substrates and exhibits in vitro quinone reductase activity. Overexpression of FQR1 in plants leads to increased levels of FQR1 protein and quinone reductase activity, indicating that FQR1 functions as a quinone reductase in vivo. In mammalian systems, glutathione S-transferases and quinone reductases are classified as phase II detoxification enzymes. We hypothesize that the auxin-inducible glutathione S-transferases and quinone reductases found in plants also act as detoxification enzymes, possibly to protect against auxin-induced oxidative stress.