Avian feathers have robust growth and regeneration capability. To evaluate the contribution of signaling molecules and pathways in these processes, we profiled gene expression in the feather follicle using an absolute quantification approach. We identified hundreds of genes that mark specific components of the feather follicle: the dermal papillae (DP) which controls feather regeneration and axis formation, the pulp mesenchyme (Pp) which is derived from DP cells and nourishes the feather follicle, and the ramogenic zone epithelium (Erz) where a feather starts to branch. The feather DP is enriched in BMP/TGF-β signaling molecules and inhibitors for Wnt signaling including Dkk2/Frzb. Wnt ligands are mainly expressed in the feather epithelium and pulp. We find that while Wnt signaling is required for the maintenance of DP marker gene expression and feather regeneration, excessive Wnt signaling delays regeneration and reduces pulp formation. Manipulating Dkk2/Frzb expression by lentiviral-mediated overexpression, shRNA-knockdown, or by antibody neutralization resulted in dual feather axes formation. Our results suggest that the Wnt signaling in the proximal feather follicle is fine-tuned to accommodate feather regeneration and axis formation.

Chemotherapeutic agents induce complex tissue responses in vivo and damage normal organ functions. Here we use the feather follicle to investigate details of this damage response. We show that cyclophosphamide treatment, which causes chemotherapy-induced alopecia in mice and man, induces distinct defects in feather formation: feather branching is transiently and reversibly disrupted, thus leaving a morphological record of the impact of chemotherapeutic agents, whereas the rachis (feather axis) remains unperturbed. Similar defects are observed in feathers treated with 5-fluorouracil or taxol but not with doxorubicin or arabinofuranosyl cytidine (Ara-C). Selective blockade of cell proliferation was seen in the feather branching area, along with a downregulation of sonic hedgehog (Shh) transcription, but not in the equally proliferative rachis. Local delivery of the Shh inhibitor, cyclopamine, or Shh silencing both recapitulated this effect. In mouse hair follicles, those chemotherapeutic agents that disrupted feather formation also downregulated Shh gene expression and induced hair loss, whereas doxorubicin or Ara-C did not. Our results reveal a mechanism through which chemotherapeutic agents damage rapidly proliferating epithelial tissue, namely via the cell population-specific, Shh-dependent inhibition of proliferation. This mechanism may be targeted by future strategies to manage chemotherapy-induced tissue damage.

Photoperiod-sensitive plants such as soybean (Glycine max) often face threats from herbivorous insects throughout their whole growth period and especially during flowering; however, little is known about the relationship between plant flowering and insect resistance. Here, we used gene editing, multiple omics, genetic diversity and evolutionary analyses to confirm that the calcium-dependent protein kinase GmCDPK38 plays a dual role in coordinating flowering time regulation and insect resistance of soybean. Haplotype 2 (Hap2)-containing soybeans flowered later and were more resistant to the common cutworm (Spodoptera litura Fabricius) than those of Hap3. gmcdpk38 mutants with Hap3 knocked out exhibited similar flowering and resistance phenotypes as Hap2. Knocking out GmCDPK38 altered numerous flowering- and resistance-related phosphorylated proteins, genes, and metabolites. For example, the S-adenosylmethionine synthase GmSAMS1 was posttranslationally upregulated in the gmcdpk38 mutants. GmCDPK38 has abundant genetic diversity in wild soybeans and was likely selected during soybean domestication. We found that Hap2 was mostly distributed at low latitudes and had a higher frequency in cultivars than in wild soybeans, while Hap3 was widely selected at high latitudes. Overall, our results elucidated that the two distinct traits (flowering time and insect resistance) are mediated by GmCDPK38.

Plants have evolved complex defense mechanisms to withstand insect attack. Identification of plant endogenous insect resistance genes is of great significance for understanding plant–herbivore interactions and improving crop insect resistance. Soybean (Glycine max (L.) Merr.) is an important crop that is often attacked by the common cutworm (CCW) (Spodoptera litura Fabricius). In this study, based on our transcriptomic data, the gene GmVQ58, encoding a FxxxVQxxTG (VQ) motif-containing protein, was cloned and characterized. This gene showed the highest expression in the leaves and roots and was up-regulated significantly after CCW attack. Constitutive expression of GmVQ58 rescued the susceptibility of an Arabidopsis mutant to CCW, and interference of GmVQ58 in soybean hairy roots enhanced the resistance to CCW. Furthermore, GmVQ58 was localized to the nucleus and physically interacted with the transcription factor GmWRKY32. The expression of two defense-related genes, GmN:IFR and GmVSPβ, was up-regulated in GmVQ58-RNAi lines. Additionally, the promoter region of GmVQ58 was likely selected during domestication, resulting in different expression patterns in cultivated soybeans relative to wild soybeans. These results suggest that silencing GmVQ58 confers soybean resistance to CCW.

Background: Low plasma vitamin A levels increases the risk of neonates' morbidity. However, the relationship between umbilical cord blood (UCB) vitamin A levels and late-preterm infant (LPI) consequences is inconclusive. Herein, we attempted to clarify the association between UCB vitamin A levels and LPI morbidities. Methods: We conducted a prospective cohort study of 208 LPI (from 34+0 to 36+6 weeks gestational age) between January 1, 2014 and June 30, 2015. UCB specimens were collected shortly after birth, and vitamin A levels were determined by enzyme-linked immunosorbent assay. Jaundice, sepsis, respiratory distress syndrome, bronchopulmonary dysplasia, necrotizing enterocolitis, and death were recorded. Results: Prevalence of low UCB vitamin A level <0.7 μmol/L was 37.5% in LPI. Cesarean section was an independent risk factor of UCB vitamin A level < 0.7 μmol/L. Nevertheless, UCB vitamin A levels did not correlate with gestational age, birthweight, and gender. UCB vitamin A level < 0.7 μmol/L was not an independent risk factor for hospitalization, oxygen supplementation, hyperbilirubinemia, sepsis and respiratory distress syndrome. However, cesarean section, gestational age < 35 weeks and birthweight < 2500 g were independent risk factors for hospitalization and RDS. In addition, cesarean section increased the risk of oxygen supplementation, while gestational age < 35 weeks increased the risk of hyperbilirubinemia. Conclusions: Cesarean section delivery is an independent risk factor of low UCB vitamin A levels, and increases the risk of RDS. On the basis of our results, there is no association between low vitamin A levels and morbidity of late-preterm infants, including hyperbilirubinemia, sepsis and respiratory distress syndrome. Trial registration: Not applicable. Background Late-preterm infants (LPI) (with gestational age between 34+0 and 36+6 weeks) is common in preterm infants. LPI has a higher morbidity of apnea, respiratory distress, kernicterus [1], and mortality rates when compared to term infants [2, 3]. Pediatricians are responsible for caring for