Solidago canadensis is native to North America, but has become a noxious invasive plant in China. We know only a little about its invasion history and the effects of introductions on its genetic composition. Here, we investigated genetic variation and structure between 15 North American and 13 Chinese populations of S. canadensis using AFLP makers. Four AFLP loci suggested relatively high genetic diversity of this weed and similar genetic variation between the invasive range and the native range. Most genetic variation was within populations across two ranges, but the Chinese range had a higher degree of among-population variation than the North American range. Multiple tests, including Bayesian assignment, UPGMA analysis, PCoA and analysis of 'isolation by distance', showed that the Chinese populations originated from at least two distinct native sources and that secondary introduction or dispersal should be common in China. Also, North American populations were possibly a single genetic group. Overall, S. canadensis in China was probably founded from multiple introductions and then spread through long-distance dispersal associated with human activities. Genetic variability in the species in the invaded range appears to have favoured establishment and spread and may well provide a challenge to successful control.

Previously, we identified SETD2 loss-of-function mutations in 22% of MLL-rearranged (MLLr) acute leukemia patients, implicating a mechanism for cooperativity between SETD2 mutations and MLL fusions. However, the detailed mechanism of how SETD2-H3K36me3 downregulation accelerates MLLr leukemia remains unclear. Here, we show that in MLLr leukemia, both H3K79me2 and H3K36me3 are aberrantly elevated and co-enriched in a group of genes. SETD2 inactivation leads to a global reduction of H3K36me3 and a further elevation of H3K79me2, but does not change the expression of known MLL fusiontarget genes. Instead, this pattern of histone changes is associated with transcriptional deregulation of a novel set of genes; downregulating tumor suppressors (for example, ASXL1) and upregulating oncogenes (for example, ERG). Taken together, our findings reveal a global crosstalk between the oncogenic DOT1L-H3K79me2 axis and the tumor suppressive SETD2-H3K36me3 axis in gene regulation, provide molecular insights into how SETD2 mutations accelerate MLLr leukemogenesis through differential regulation of additional tumor suppressors and oncogenes.

Aberrant activation of the three-amino-acid-loop extension (TALE) homeobox gene MEIS1 shortens the latency and accelerates the onset and progression of acute leukemia, yet the molecular mechanism underlying persistent activation of the MEIS1 gene in leukemia remains poorly understood. Here we used a combined comparative genomics analysis and an in vivo transgenic zebrafish assay to identify 6 regulatory DNA elements that are able to direct GFP expression in a spatiotemporal manner during zebrafish embryonic hematopoiesis. Analysis of chromatin characteristics and regulatory signatures suggest that many of these predicted elements are potential enhancers in mammalian hematopoiesis. Strikingly, one of the enhancer elements (E9) is a frequent integration site in retroviral induced mouse acute leukemia. The genomic region corresponding to enhancer E9 is differentially marked by H3K4 mono-methylation and H3K27 acetylation, hallmarks of active enhancers, in multiple leukemia cell lines. Decreased enrichment of these histone marks is associated with downregulation of MEIS1 expression during hematopoietic differentiation. Furthermore, MEIS1/HOXA9 transactivate this enhancer via a conserved binding motif in vitro, and participate in an autoregulatory loop that modulates MEIS1 expression in vivo. Our results suggest that an intronic enhancer regulates the expression of MEIS1 in hematopoiesis and contributes to its aberrant expression in acute leukemia.

ABSTRACT. Hagenia abyssinica (Bruce) J.F. Gmel is an endangered tree species endemic to the high mountains of tropical Africa. We used Illumina paired-end technology to sequence its nuclear genome, aiming at creating the first genomic data library and developing the first set of genomic microsatellites. Seventeen microsatellite markers were validated in 24 individuals. The average number of alleles per locus was 7.6, while the observed and expected heterozygosities ranged from 0.000 to 0.958 and from 0.354 to 0.883, respectively. These polymorphic markers will be used as tools for further molecular studies to facilitate formulation of appropriate conservation strategies for this species.

No abstract

ABSTRACT. Davidia involucrata, reputed to be a "living fossil" in the plant kingdom, is a relict tree endemic to China. Extant natural populations are diminishing due to anthropogenic disturbance. In order to understand its ability to survive in a range of climatic conditions and to design conservation strategies for this endangered species, we developed genic simple sequence repeats (SSRs) from mRNA transcripts. In total, 142,950 contigs were assembled. Of these, 30,411 genic SSR loci were discovered and 12,208 primer pairs were designed. Dinucleotides were the most common (77.31%) followed by trinucleotides (16.44%). Thirteen randomly selected primers were synthesized and validated using 24 individuals of D. involucrata. The markers displayed high polymorphism with the number of alleles per locus ranging from 3 to 12 and the observed and expected heterozygosities ranging from 0.083 to 1.0 and 0.102 to 0.69, respectively. This large expressed sequence tag dataset and the novel SSR markers will be key tools in comparative studies that may reveal the adaptive evolution, population structure, and resolve the genetic diversity in this endangered species.