Journal of Biology最新文献

The presence of mammary glands is the defining morphological feature of mammals. The recent assembly of the bovine genome and a report in Genome Biology that links the milk and lactation data of bovine and other mammalian genomes will help biologists investigate this economically and medically important feature.

A recent paper in BMC Developmental Biology describes the development of the annulus of the mouse sperm cell, but much remains to be learnt about sperm cells despite their importance in human fertility.

The aryl hydrocarbon receptor is a ligand-activated transcriptional regulator that binds dioxin and other exogenous contaminants and is responsible for their toxic effects, including immunosuppression. New evidence suggests, however, that the aryl hydrocarbon receptor has a physiological role in the immune system, and the immunosuppressive effects of dioxin may reflect a more subtle disruption of the regulatory interactions between immune cells.

Zebrafish are a powerful system for studying the early embryonic events that form the skull and face, as a model for human craniofacial birth defects such as cleft palate. Signaling pathways that pattern the pharyngeal arches (which contain skeletal precursors of the palate, as well as jaws and gills) are discussed in light of a recent paper in BMC Developmental Biology on requirements for Hedgehog signaling in craniofacial development.

The individual 'validation' experiments typically included in papers reporting genome-scale studies often do not reflect the overall merits of the work.

Apoptosis appears to be a carefully orchestrated process for the ordered dismantling of cells. A recent paper in BMC Developmental Biology shows that the disassembly of adherens junctions during apoptosis in Drosophila is progressive and requires the amino-terminal cleavage of the beta-catenin Armadillo by the apoptotic effector caspase DrICE.

Information on how genomic information from fish to human encodes the same tissues has until now emerged one gene at a time. The study published in this issue now provides lists of genes and their expression levels for 20 vertebrate tissues spanning 450 million years of vertebrate evolution. It reveals a core set of genes with similar tissue-expression patterns yet no common regulatory signatures--a gene-expression paradox.

Sensory identity usually remains constant across a large intensity range. Vertebrates use lateral inhibition to match the sensitivity of retinal ganglion cells to the intensity of light. A new study published in Journal of Biology suggests that lateral inhibition in the Drosophila antennal lobe is similarly required for concentration-invariant perception of odors.

Background: In addition to progressive CD4(+) T cell immune deficiency, HIV infection is characterized by generalized immune activation, thought to arise from increased microbial exposure resulting from diminishing immunity.

Results: Here we report that, in a virus-free mouse model, conditional ablation of activated CD4(+) T cells, the targets of immunodeficiency viruses, accelerates their turnover and produces CD4(+) T cell immune deficiency. More importantly, activated CD4(+) T cell killing also results in generalized immune activation, which is attributable to regulatory CD4(+) T cell insufficiency and preventable by regulatory CD4(+) T cell reconstitution. Immune activation in this model develops independently of microbial exposure. Furthermore, microbial translocation in mice with conditional disruption of intestinal epithelial integrity affects myeloid but not T cell homeostasis.

Conclusions: Although neither ablation of activated CD4(+) T cells nor disruption of intestinal epithelial integrity in mice fully reproduces every aspect of HIV-associated immune dysfunction in humans, ablation of activated CD4(+) T cells, but not disruption of intestinal epithelial integrity, approximates the two key immune alterations in HIV infection: CD4(+) T cell immune deficiency and generalized immune activation. We therefore propose activated CD4(+) T cell killing as a common etiology for both immune deficiency and activation in HIV infection.