Publications by authors named "Heather Maylor-Hagen"

Failure of homologous chromosomes to recombine is arguably the most important cause of human meiotic nondisjunction, having been linked to numerous autosomal and sex chromosome trisomies of maternal origin. However, almost all information on these "exchangeless" homologs has come from genetic mapping studies of trisomic conceptuses, so the incidence of this defect and its impact on gametogenesis are not clear. If oocytes containing exchangeless homologs are selected against during meiosis, the incidence may be much higher in developing germ cells than in zygotes.

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Meiotic recombination is initiated by programmed double strand breaks (DSBs), only a small subset of which are resolved into crossovers (COs). The mechanism determining the location of these COs is not well understood. Studies in plants, fungi, and insects indicate that the same genomic regions are involved in synaptic initiation and COs, suggesting that early homolog alignment is correlated with the eventual resolution of DSBs as COs.

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Article Synopsis
  • - The study investigates severe Lyme arthritis in C3H mice infected with Borrelia burgdorferi, focusing on the role of type I interferon (IFN) and how it contributes to the disease process.
  • - Researchers used genetically modified mice lacking the type I IFN receptor to analyze how various joint cells contribute to the IFN response, revealing that myeloid cells, endothelial cells, and fibroblasts played key roles.
  • - The findings highlight complex interactions between different cell types in the joint that trigger the IFN response, suggesting similar mechanisms could be relevant for other diseases linked to type I IFN, like lupus and certain rheumatoid arthritis forms.
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We recently discovered a critical role for type I interferon (IFN) in the development of murine Lyme arthritis. Borrelia burgdorferi-mediated induction of IFN-responsive genes by bone marrow-derived macrophages (BMDMs) was dependent upon a functional type I IFN receptor but independent of Toll-like receptor 2 (TLR2), TLR4, TLR9, and the adapter molecule MyD88. We now demonstrate that induction of the IFN transcriptional profile in B.

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