Background: The involvement of small RNAs in cotton fiber development is under explored. The objective of this work was to directly clone, annotate, and analyze small RNAs of developing ovules to reveal the candidate small interfering RNA/microRNAs involved in cotton ovule and fiber development.

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Molecular markers associated withWber development traits have the potential to play a key role in understanding of cotton Wber development. Seventeen SSRs out of 304 markers tested from MGHES (EST-SSR), JESPR (genomic SSR), and TMB (BAC-derived SSR) collections showed signiWcant linkage associations (using a Kurskal-Wallis non-parametric test) with lint percentage QTL in a set of recombinant inbred cotton lines (RILs) segregating for lint percentage. The permutation test of these potential markers associated with lint percentage QTL(s) determined that 12 SSR markers have stable estimates, exceeding empirically chosen threshold signiWcance values at or above = 0.01. Interval mapping demonstrated that 9 SSRs with stable critical LOD threshold values at = 0.01 have signiWcant QTL eVect. Multiple QTL-mapping (MQM) revealed that at least, two highly signiWcant Wber development QTLs exist around regions TMB0471 and MGHES-31 (explained about 23-59% of the phenotypic variation of lint percentage) and around markers MGHES-31 and TMB0366 (accounted for 5.4-12.5% phenotypic variation of lint percentage). These markers, in particular Wber-speciWc EST-SSRs, might be the possible 'candidate' loci contributing for Wber development in cotton. BAC-derived SSRs associated with Wber trait are the possible markers that are useful for the identiWcation of physical genomic contigs that contain Wber development genes. Several lint percentage trait associated SSR markers have been located to chromosomes 12, 18, 23, and 26 using deletion analysis in aneuploid chromosome substitution lines. Outcomes of the work may prove useful in understanding I. Y. Abdurakhmonov and S. Saha contributed equally to the work

Wild cotton germplasm resources are largely underutilized because of photoperiod-dependent flowering of "exotic" cottons. The objectives of this work were to explore the genome-wide effect of induced mutation in photoperiod-converted induced cotton mutants, estimating the genetic change between mutant and wild-type cottons using simple sequence repeats (SSRs) as well as understand the pattern of SSR mutation in induced mutagenesis. Three groups of photoperiod-converted radiomutants ((32)P) including their wild-type parental lines, A- and D-genome diploids, and typically grown cotton cultivars were screened with 250 cotton SSR primer pairs. Forty SSRs revealed the same SSR mutation profile in, at least, 2 independent mutant lines that were different from the original wild types. Induced mutagenesis both increased and decreased the allele sizes of SSRs in mutants with the higher mutation rate in SSRs containing dinucleotide motifs. Genetic distance obtained based on 141 informative SSR alleles ranged from 0.09 to 0.60 in all studied cotton genotypes. Genetic distance within all photoperiod-converted induced mutants was in a 0.09-0.25 range. The genetic distance among photoperiod-converted mutants and their originals ranged from 0.28 to 0.50, revealing significant modification of mutants from their original wild types. Typical Gossypium hirsutum cultivar, Namangan-77, revealed mutational pattern similar to induced radiomutants in 40 mutated SSR loci, implying possible pressure to these SSR loci not only in radiomutagenesis but also during common breeding process. Outcomes of the research should be useful in understanding the photoperiod-related mutations, and markers might help in mapping photoperiodic flowering genes in cotton.

This study was conducted to test whether ginsenoside F2 can reduce hair loss by influencing sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP) and the transforming growth factor beta (TGF-β) pathway of apoptosis in dihydrotestosterone (DHT)-treated hair cells and in a DHT-induced hair loss model in mice. Results for ginsenoside F2 were compared with finasteride. DHT inhibits proliferation of hair cells and induces androgenetic alopecia and was shown to activate an apoptosis signal pathway both in vitro and in vivo. The cell-based 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showed that the proliferation rates of DHT-treated human hair dermal papilla cells (HHDPCs) and HaCaTs increased by 48% in the ginsenoside F2-treated group and by 12% in the finasteride-treated group. Western blot analysis showed that ginsenoside F2 decreased expression of TGF-β2 related factors involved in hair loss. The present study suggested a hair loss related pathway by changing SCAP related apoptosis pathway, which has been known to control cholesterol metabolism. SCAP, sterol regulatory elementbinding protein (SREBP) and caspase-12 expression in the ginsenoside F2-treated group were decreased compared to the DHT and finasteride-treated group. C57BL/6 mice were also prepared by injection with DHT and then treated with ginsenoside F2 or finasteride. Hair growth rate, density, thickness measurements and tissue histotological analysis in these groups suggested that ginsenoside F2 suppressed hair cell apoptosis and premature entry to catagen more effectively than finasteride. Our results indicated that ginsenoside F2 decreased the expression of TGF-β2 and SCAP proteins, which have been suggested to be involved in apoptosis and entry into catagen. This study provides evidence those factors in the SCAP pathway could be targets for hair loss prevention drugs.