Characterization of a novel dsRNA element in the pine endophytic fungus Diplodia scrobiculata

Diplodia scrobiculata and Diplodia pinea are endophytic fungi associated with dieback and cankers of mainly Pinus spp. in many parts of the world. These two fungi are closely related and have, in the past, been considered to represent two morphological forms (A and B morphotypes) of D. pinea. dsRNA elements are known to occur in both D. scrobiculata and D. pinea. Two dsRNA elements from D. pinea, SsRV1 and SsRV2, have been characterized previously. The aim of this study was to characterize a third dsRNA element that is most commonly associated with D. scrobiculata and to determine its phylogenetic relationship to other mycoviruses. The 5018-bp genome of this element was sequenced, and it is referred to as D. scrobiculata RNA virus 1, or DsRV1. It has two open reading frames (ORFs), one of which codes for a putative polypeptide with a high degree of similarity to proteins of the vacuolar protein-sorting (VPS) machinery, and the other for an RNA-dependent RNA polymerase (RdRp). Phylogenetic comparisons based on amino acid sequence alignments of the RdRp revealed that DsRV1 is closely related to a dsRNA element isolated from Phlebiopsis gigantea (PgV2), and they grouped separately from virus families in which mycoviruses have previously been described. Although D. pinea and D. scrobiculata are closely related, DsRV1 does not share high sequence identity with SsRV1 or SsRV2, and they probably have different recent evolutionary origins

Oligodendrocyte Fate after Spinal Cord Injury

Oligodendrocytes (OLs) are particularly susceptible to the toxicity of the acute lesion environment after spinal cord injury (SCI). They undergo both necrosis and apoptosis acutely, with apoptosis continuing at chronic time points. Loss of OLs causes demyelination and impairs axon function and survival. In parallel, a rapid and protracted OL progenitor cell proliferative response occurs, especially at the lesion borders. Proliferating and migrating OL progenitor cells differentiate into myelinating OLs, which remyelinate demyelinated axons starting at 2 weeks post-injury. The progression of OL lineage cells into mature OLs in the adult after injury recapitulates development to some degree, owing to the plethora of factors within the injury milieu. Although robust, this endogenous oligogenic response is insufficient against OL loss and demyelination. First, in this review we analyze the major spatial–temporal mechanisms of OL loss, replacement, and myelination, with the purpose of highlighting potential areas of intervention after SCI. We then discuss studies on OL protection and replacement. Growth factors have been used both to boost the endogenous progenitor response, and in conjunction with progenitor transplantation to facilitate survival and OL fate. Considerable progress has been made with embryonic stem cell-derived cells and adult neural progenitor cells. For therapies targeting oligogenesis to be successful, endogenous responses and the effects of the acute and chronic lesion environment on OL lineage cells must be understood in detail, and in relation, the optimal therapeutic window for such strategies must also be determined