Cotton is the leading natural fiber crop in the world. Cotton seeds are also an important oil and protein source. However, enhancement of fiber abundance usually leads to a smaller seed. Thus, it has become a challenge for cotton breeding to concurrently increase fiber yield and seed yield. To improve cotton yield, we elevated the endogenous cytokinin level in transgenic cotton by constitutive suppression of cytokinin dehydrogenase (CKX), a key negative regulator controlling endogenous cytokinin in plants. The slightly and moderately suppressed transgenic cotton plants showed normal growth and development, while the severely suppressed plants exhibited a typical cytokinin-overproduction alteration. The suppression of CKX led to an enhancement of endogenous cytokinins in transgenic cotton plants. Total cytokinins in moderately suppressed lines, CR-3 and CR-6, increased by 20.4 and 55.5 % respectively, and that in the severely suppressed line (CR-13) increased by 134.2 % compared to the wild type. The moderately suppressed lines showed a delay in leaf senescence, higher photosynthesis, more fruiting branches and bolls, and bigger seed size. Field trials showed that seed yield and lint yield of the moderately suppressed CR-6 line increased by 15.4 and 20.0 %, respectively. Meanwhile, the enhanced cytokinin level in transgenic cottons did not show significant influence on fiber qualities. Our data demonstrated that CKX is a promising gene for crop yield improvement.

Auxin-dependent cell expansion is crucial for initiation of fiber cells in cotton (Gossypium hirsutum), which ultimately determines fiber yield and quality. However, the regulation of this process is far from being well understood. In this study, we demonstrate an antagonistic effect between cytokinin (CK) and auxin on cotton fiber initiation. In vitro and in planta experiments indicate that enhanced CK levels can reduce auxin accumulation in the ovule integument, which may account for the defects in the fiberless mutant xu142fl. In turn, supplementation with auxin can recover fiber growth of CK-treated ovules and mutant ovules. We further found that GhPIN3a is a key auxin transporter for fiber-cell initiation and is polarly localized to the plasma membranes of non-fiber cells, but not to those of fiber cells. This polar localization allows auxin to be transported within the ovule integument while specifically accumulating in fiber cells. We show that CKs antagonize the promotive effect of auxin on fiber cell initiation by undermining asymmetric accumulation of auxin in the ovule epidermis through down-regulation of GhPIN3a and disturbance of the polar localization of the protein.

Cotton fibers are seed trichomes that make cotton unique compared with other plants. At anthesis, IAA, a major auxin in plants, accumulates in the fiber cell to promote cell initiation. However, many important aspects of this process are not clear. Here, auxin distribution patterns indicated by auxin-dependent DR5::GUS (β-glucuronidase) expression in cotton ovules were studied during fiber cell differentiation and cell initiation [–2 to 2 DPA (days post-anthesis)]. The nucellus and fiber cell were two major sites where auxin accumulates. The accumulation in the nucellus started from –1 DPA, and that in fiber cells from 0 DPA. Immunolocalization analysis further suggests that the IAA accumulation in fiber initials began before flower opening. Furthermore, we demonstrate that accumulated IAA in fiber initials was mainly from efflux transport and not from in situ synthesis. Eleven auxin efflux carrier (GhPIN) genes were identified, and their expression during ovule and fiber development was investigated. Ovule-specific suppression of multiple GhPIN genes in transgenic cotton inhibited both fiber initiation and elongation. In 0 DPA ovules, GhPIN3a, unlike other GhPIN genes, showed additional localization of the transcript in the outer integument. Collectively, these results demonstrate the important role of GhPIN-mediated auxin transport in fiber-specific auxin accumulation for fiber initiation.

Many toxic secondary metabolites produced by phytopathogens can subvert host immunity, and some of them are recognized as pathogenicity factors. Fusarium head blight and Verticillium wilt are destructive plant diseases worldwide. Using toxins produced by the causal fungi Fusarium graminearum and Verticillium dahliae as screening agents, here we show that the Arabidopsis P4 ATPases AtALA1 and AtALA7 are responsible for cellular detoxification of mycotoxins. Through AtALA1-/AtALA7-mediated vesicle transport, toxins are sequestered in vacuoles for degradation. Overexpression of AtALA1 and AtALA7 significantly increases the resistance of transgenic plants to F. graminearum and V. dahliae, respectively. Notably, the concentration of deoxynivalenol, a mycotoxin harmful to the health of humans and animals, was decreased in transgenic Arabidopsis siliques and maize seeds. This vesicle-mediated cell detoxification process provides a strategy to increase plant resistance against different toxin-associated diseases and to reduce the mycotoxin contamination in food and feed.