Cover crops (CCs) can provide multiple soil, agricultural production, and environmental benefits. However, a better understanding of such potential ecosystem services is needed. We summarized the current state of knowledge of CC effects on soil C stocks, soil erosion, physical properties, soil water, nutrients, microbial properties, weed control, crop yields, expanded uses, and economics and highlighted research needs. Our review indicates that CCs are multifunctional. Cover crops increase soil organic C stocks (0.1–1 Mg ha−1 yr−1) with the magnitude depending on biomass amount, years in CCs, and initial soil C level. Runoff loss can decrease by up to 80% and sediment loss from 40 to 96% with CCs. Wind erosion potential also decreases with CCs, but studies are few. Cover crops alleviate soil compaction, improve soil structural and hydraulic properties, moderate soil temperature, improve microbial properties, recycle nutrients, and suppress weeds. Cover crops increase or have no effect on crop yields but reduce yields in water‐limited regions by reducing available water for the subsequent crops. The few available studies indicate that grazing and haying of CCs do not adversely affect soil and crop production, which suggests that CC biomass removal for livestock or biofuel production can be another benefit from CCs. Overall, CCs provide numerous ecosystem services (i.e., soil, crop–livestock systems, and environment), although the magnitude of benefits is highly site specific. More research data are needed on the (i) multi‐functionality of CCs for different climates and management scenarios and (ii) short‐ and long‐term economic return from CCs.

Summary We report that p73 is expressed in multiciliated cells (MCCs), is required for MCC differentiation, and directly regulates transcriptional modulators of multiciliogenesis. Loss of ciliary biogenesis provides a unifying mechanism for many phenotypes observed in p73 knockout mice including hydrocephalus, hippocampal dysgenesis, sterility and chronic inflammation/infection of lung, middle ear and sinus. Through p73 and p63 ChIP-seq using murine tracheal cells, we identified over 100 putative p73 target genes that regulate MCC differentiation and homeostasis. We validated Foxj1, a transcriptional regulator of multiciliogenesis, and many other cilia-associated genes as direct target genes of p73 and p63. We show p73 and p63 are co-expressed in a subset of basal cells, and suggest that p73 ‘marks’ these cells for MCC differentiation. In sum, p73 is essential for MCC differentiation, functions as a critical regulator of a transcriptome required for MCC differentiation and, like p63, has an essential role in development of tissues.

Single-layered embryonic skin either stratifies to form epidermis or responds to Wnt signaling (stabilized β-catenin) to form hair follicles. Postnatally, stem cells continue to differentially use Wnt signaling in long-term tissue homeostasis. We have discovered that embryonic progenitor cells and postnatal hair follicle stem cells coexpress Tcf3 and Tcf4, which can act as transcriptional activators or repressors. Using loss-of-function studies and transcriptional analyses, we uncovered consequences to the absence of Tcf3 and Tcf4 in skin that only partially overlap with those caused by β-catenin deficiency. We established roles for Tcf3 and Tcf4 in long-term maintenance and wound repair of both epidermis and hair follicles, suggesting that Tcf proteins have both Wnt-dependent and Wnt-independent roles in lineage determination.Members of the Lef1 and Tcf family of DNA binding proteins bind β-catenin and transactivate Wnt target genes 1 . We previously discovered that Tcf3 is essential for gastrulation, where it differs from other Lef1 and Tcf binding proteins in acting not only in the presence but also in the apparent absence of Wnt signaling [2][3][4] . In embryonic skin, Tcf3 and Lef1 are expressed in basal progenitors 4,5 . As morphogenesis proceeds, Tcf3 becomes restricted to the early hair follicle 'bulge' region, a site where slow-cycling multipotent stem cells will reside, whereas Lef1 becomes confined to the base of the growing hair follicle, where committed, transitamplifying matrix cells and precortical cells differentiate to produce the hair 4,6 . In postnatal skin, Tcf3 remains a faithful marker of hair follicle stem cells: its expression is maintained both in the bulge and in the outer root sheath (ORS) cells that trail down from the bulge. The ORS cells are thought to represent activated stem cells in transit to the hair follicle bulb, where they fuel production of the matrix cells, hair shaft and surrounding channel [6][7][8] . We have shown that bulge stem cell activation is dependent on Wnt signaling and stabilized β-catenin, whereas Note: Supplementary information is available on the Nature Genetics website.Reprints and permissions information is available online at http://npg.nature.com/reprintsandpermissions/. AUTHOR CONTRIBUTIONSH.N. designed and conducted experiments, analyzed data and wrote the paper. B.J.M. generated the Tcf3 cKO mice. M.R. conducted the microarray analysis. L.P. conducted the skin grafting. M.N. and T.M.S. provided technical assistance. H.A.P. conducted the histological analysis. E.F. designed experiments, analyzed data and wrote the paper. All authors read and contributed to the manuscript. during the resting stage of the hair cycle, Tcf3 persists in the apparent absence of nuclear β-catenin 2,5,9 . NIH Public AccessLef1 and Tcf DNA binding proteins have not been identified in resident stem cells of epidermis or sebaceous glands. However, expression of a dominant-negative Lef1 promotes sebaceous gland cell proliferation and differentiation 2,10 , and ectopic ind...

Replacement of fallow in crop–fallow systems with cover crops (CCs) may improve soil properties. We assessed whether replacing fallow in no‐till winter wheat (Triticum aestivum L.)–fallow with winter and spring CCs for 5 yr reduced wind and water erosion, increased soil organic carbon (SOC), and improved soil physical properties on a Ulysses silt loam (fine‐silty, mixed, superactive, mesic Aridic Haplustolls) in the semiarid central Great Plains. Winter triticale (×Triticosecale Wittm.), winter lentil (Lens culinaris Medik.), spring lentil, spring pea (Pisum sativum L. ssp.), and spring triticale CCs were compared with wheat–fallow and continuous wheat under no‐till management. We also studied the effect of triticale haying on soil properties. Results indicate that spring triticale and spring lentil increased soil aggregate size distribution, while spring lentil reduced the wind erodible fraction by 1.6 times, indicating that CCs reduced the soil's susceptibility to wind erosion. Cover crops also increased wet aggregate stability and reduced runoff loss of sediment, total P, and NO3–N. After 5 yr, winter and spring triticale increased SOC pool by 2.8 Mg ha–1 and spring lentil increased SOC pool by 2.4 Mg ha–1 in the 0‐ to 7.5‐cm depth compared with fallow. Triticale haying compared with no haying for 5 yr did not affect soil properties. Nine months after termination, CCs had, however, no effects on soil properties, suggesting that CC benefits are short lived in this climate. Overall, CCs, grown in each fallow phase in no‐till, can reduce soil erosion and improve soil aggregation in this semiarid climate.

Oncogenic EGFR mutations are found in 10-35% of lung adenocarcinomas. Such mutations, which present most commonly as small in-frame deletions in exon 19 or point mutations in exon 21 (L858R), confer sensitivity to EGFR tyrosine kinase inhibitors (TKIs). In analyzing the tumor from a 33-year-old male never smoker, we identified a novel EGFR alteration in lung cancer: EGFR exon 18-25 kinase domain duplication (EGFR-KDD). Through analysis of a larger cohort of tumor samples, we detected additional cases of EGFR-KDD in lung, brain, and other cancers. In vitro, EGFR-KDD is constitutively active, and computational modeling provides potential mechanistic support for its auto-activation. EGFR-KDD-transformed cells are sensitive to EGFR TKIs and, consistent with these in vitro findings, the index patient had a partial response to the EGFR TKI, afatinib. The patient eventually progressed, at which time, re-sequencing revealed an EGFR-dependent mechanism of acquired resistance to afatinib, thereby validating EGFR-KDD as a driver alteration and therapeutic target.