The Owen mitochondrial genome in sugar beet (Beta vulgaris L.): possible mechanisms of extensive rearrangements and the origin of the mitotype-unique regions.

The mitochondrial genomes of normal fertile and male-sterile (Owen CMS) cytoplasms of sugar beet are highly rearranged relative to each other and dozens of inversional recombinations and other reshuffling events must be postulated to interconvert the two genomes. In this paper, a comparative analysis of the entire nucleotide sequences of the two genomes revealed that most of the inversional recombinations involved short repeats present at their endpoints. Attention was also focused on the origin of the Owen CMS-unique mtDNA regions, which occupy 13.6% of the Owen genome and are absent from the normal mtDNA. BLAST search was performed to assign the sequences, and as a result, 7.6% of the unique regions showed significant homology to previously determined mitochondrial sequences, 17.9% to nuclear DNA, 4.6% to mitochondrial episomes, and 0.1% to plastid DNA. Southern blot analysis revealed that additional sequences of nuclear origin may be included within the unique regions. We also found that the copies of many short repeat families are scattered throughout the unique regions. This suggests that, in addition to the incorporation of foreign DNAs, extensive duplication of short repetitive sequences and continued scrambling of mtDNA sequences may be implicated in the generation of the Owen CMS-unique regions.

Different cytokines induce surface lymphotoxin-alphabeta on IL-7 receptor-alpha cells that differentially engender lymph nodes and Peyer's patches.

The formation of lymph nodes (LN) and Peyer's patches (PP) can be distinguished by the requirement of RANK for LN but not IL-7R(alpha), which is essential for PP development. However, lymphotoxin-alphabeta (LT(alpha)beta) signaling is required for both organs. The cellular basis underlying this dichotomy was revealed by the finding that the fetal IL-7R(alpha)(+) population responded equally well to IL-7 and RANKL to express LT(alpha)beta. IL-7R(alpha)(+) cells harvested from TRAF6(-/-) embryos expressed LTalphabeta in response to IL-7 but not RANKL, demonstrating that the RANK-TRAF6 signaling pathway regulates LT(alpha)beta expression in LN but not in PP. Soluble IL-7 administered to TRAF6(-/-) embryos was sufficient to restore LN genesis indicating the functional similarities of the IL-7R(alpha)(+) inducer cells for LN and PP genesis.

TRAF6-deficient mice display hypohidrotic ectodermal dysplasia.

Tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6) is an adapter protein that links signals from members of the TNFR superfamily and Toll/IL-1 receptor family to activation of transcription factors NFkappaB and AP-1. Analysis of TRAF6-deficient mice revealed that TRAF6 is essential for normal bone formation and establishment of immune and inflammatory systems. Here we report that TRAF6 deficiency results in defective development of epidermal appendixes, including guard hair follicles, sweat glands, sebaceous glands of back skin, and modified sebaceous glands such as meibomian glands, anal glands, and preputial glands. Except the sebaceous gland impairment, these abnormal phenotypes are identical to those observed in Tabby (Ta), downless (dl), and crinkled (cr) mice, which are models of hypohidrotic (anhidrotic) ectodermal dysplasia in human. beta-catenin and mucosal addressin cell adhesion molecule-1, an early marker of developing guard-hair follicles is absent in the skin of TRAF6-deficient embryos. Thus, TRAF6 is essential for development of epidermal appendixes. TRAF6 does not associate with the cytoplasmic tail of the dl protein (DL)/ectodysplasin receptor (EDAR) receptor, which, when mutated, results in hypohidrotic (anhidrotic) ectodermal dysplasia. However, TRAF6 associates with X-linked ectodysplasin-A2 receptor (XEDAR) and TNFR super family expressed on the mouse embryo (TROY/toxicity and JNK inducer (TAJ), which are EDAR-related members of the TNFR superfamily that are expressed at high level in epidermal appendixes. Furthermore, TRAF6 is essential for the XEDAR-mediated NFkappaB activation. Our results suggest that TRAF6 may transduce signals emanating from XEDAR or TROY/TAJ that are associated with development of epidermal appendixes.