Development and validation of SSR markers related to flower color based on full-length transcriptome sequencing in Chrysanthemum.

Chrysanthemum (Chrysanthemum moriforlium Ramat.) is one of the most popular flowers worldwide, with very high ornamental and economic values. However, the limitations of available DNA molecular markers and the lack of full genomic sequences hinder the study of genetic diversity and the molecular breeding of chrysanthemum. Here, we developed simple sequence repeat (SSR) from the full-length transcriptome sequences of chrysanthemum cultivar 'Hechengxinghuo'. A total of 11,699 SSRs with mono-, di-, tri-, tetra-, penta- and hexanucleotide repeats were identified, of which eight out of eighteen SSR loci identified based on sixteen transcripts participated in carotenoid metabolism or anthocyanin synthesis were validated as polymorphic SSR markers. These SSRs were used to classify 117 chrysanthemum accessions with different flower colors at the DNA and cDNA levels. The results showed that four SSR markers of carotenoid metabolic pathway divided 117 chrysanthemum accessions into five groups at cDNA level and all purple chrysanthemum accessions were in the group III. Furthermore, the SSR marker CHS-3, LCYE-1 and 3MaT may be related to green color and the PSY-1b marker may be related to yellow color. Overall, our work may be provide a novel method for mining SSR markers associated with specific traits.

BACH2 inhibition reverses ß cell failure in type 2 diabetes models.

Type 2 diabetes (T2D) is associated with defective insulin secretion and reduced ß cell mass. Available treatments provide a temporary reprieve, but secondary failure rates are high, making insulin supplementation necessary. Reversibility of ß cell failure is a key translational question. Here, we reverse engineered and interrogated pancreatic islet-specific regulatory networks to discover T2D-specific subpopulations characterized by metabolic inflexibility and endocrine progenitor/stem cell features. Single-cell gain- and loss-of-function and glucose-induced Ca2+ flux analyses of top candidate master regulatory (MR) proteins in islet cells validated transcription factor BACH2 and associated epigenetic effectors as key drivers of T2D cell states. BACH2 knockout in T2D islets reversed cellular features of the disease, restoring a nondiabetic phenotype. BACH2-immunoreactive islet cells increased approximately 4-fold in diabetic patients, confirming the algorithmic prediction of clinically relevant subpopulations. Treatment with a BACH inhibitor lowered glycemia and increased plasma insulin levels in diabetic mice, and restored insulin secretion in diabetic mice and human islets. The findings suggest that T2D-specific populations of failing ß cells can be reversed and indicate pathways for pharmacological intervention, including via BACH2 inhibition.