Grass pea natural variation reveals oligogenic resistance to Fusarium oxysporum f. sp. pisi.

Grass pea (Lathyrus sativus L.) is an annual legume species, phylogenetically close to pea (Pisum sativum L.), that may be infected by Fusarium oxysporum f. sp. pisi (Fop), the causal agent of fusarium wilt in peas with vast worldwide yield losses. A range of responses varying from high resistance to susceptibility to this pathogen has been reported in grass pea germplasm. Nevertheless, the genetic basis of that diversity of responses is still unknown, hampering its breeding exploitation. To identify genomic regions controlling grass pea resistance to fusarium wilt, a genome-wide association study approach was applied on a grass pea worldwide collection of accessions inoculated with Fop race 2. Disease responses were scored in this collection that was also subjected to high-throughput based single nucleotide polymorphisms (SNP) screening through genotyping-by-sequencing. A total of 5,651 high-quality SNPs were considered for association mapping analysis, performed using mixed linear models accounting for population structure. Because of the absence of a fully assembled grass pea reference genome, SNP markers' genomic positions were retrieved from the pea's reference genome v1a. In total, 17 genomic regions were associated with three fusarium wilt response traits in grass pea, anticipating an oligogenic control. Seven of these regions were located on pea chromosomes 1, 6, and 7. The candidate genes underlying these regions were putatively involved in secondary and amino acid metabolism, RNA (regulation of transcription), transport, and development. This study revealed important fusarium wilt resistance favorable grass pea SNP alleles, allowing the development of molecular tools for precision disease resistance breeding.

Genome-wide identification of microRNA signatures associated with stem/progenitor cells in Philadelphia chromosome-positive acute lymphoblastic leukemia.

Acute lymphoblastic leukemia (ALL) is a malignant transformation with uncontrolled proliferation of lymphoid precursor cells within bone marrow including a dismal prognosis after relapse. Survival of a population of quiescent leukemia stem cells (LSCs, also termed leukemia-initiating cells (LICs)) after treatment is one of the relapse reasons in Ph+ ALL patient. MicroRNAs (miRNAs) are known as highly conserved 19-24 nucleotides non-protein-coding small RNAs that regulate the expression of human genes. miRNAs are often involved in the tuning of hematopoiesis. Therefore, the deregulation of miRNA expression and function in hematopoietic cells can cause cancer and promote its progression. This is the first comprehensive analysis of miRNA expression differences between CD34+CD38- LSCs and CD34+CD38+ leukemic progenitors (LPs) from the same Ph+ B-ALL bone marrow samples using high-throughput sequencing technologies. We identified multiple differentially expressed miRNAs including hsa-miR-3143, hsa-miR-6503-3p, hsa-miR-744-3p, hsa-miR-1226-3p, hsa-miR-10a-5p, hsa-miR-4658 and hsa-miR-493-3p related to LSC and LP populations which have regulatory functions in stem-cell associated biological processes. The deregulation of these miRNAs could affect leukemogenesis, clonogenic and stemness capacities in these subpopulations of Ph+ B-ALL. Therefore, identification of these LSC associated miRNAs may improve the diagnosis and management of B-ALL. These findings may also lead to future strategies to eliminate the presence of resistant LSCs, either by induction of apoptosis or by sensitizing these cells to chemotherapy.