Leaves and floral organs are polarized along their adaxial-abaxial (dorsal-ventral) axis. In Arabidopsis, this difference is particularly obvious in the first two rosette leaves, which possess trichomes (leaf hairs) on their adaxial surface but not their abaxial surface. Mutant alleles of KANADI (KAN) were identified in a screen for mutants that produce abaxial trichomes on these first two leaves. kan mutations were originally identified as enhancers of the mutant floral phenotype of crabs claw (crc), a gene that specifies abaxial identity in carpels. Here we show that KAN is required for abaxial identity in both leaves and carpels, and encodes a nuclear-localized protein in the GARP family of putative transcription factors. The expression pattern of KAN messenger RNA and the effect of ectopically expressing KAN under the regulation of the cauliflower mosaic virus (CAMV) 35S promoter indicate that KAN may also specify peripheral identity in the developing embryo.
Loss-of-function mutations of HASTY (HST) affect many different processes in Arabidopsis development. In addition to reducing the size of both roots and lateral organs of the shoot, hstmutations affect the size of the shoot apical meristem, accelerate vegetative phase change, delay floral induction under short days, adaxialize leaves and carpels, disrupt the phyllotaxis of the inflorescence, and reduce fertility. Double mutant analysis suggests that HST acts in parallel toSQUINT in the regulation of phase change and in parallel toKANADI in the regulation of leaf polarity. Positional cloning demonstrated that HST is the Arabidopsis ortholog of the importin β-like nucleocytoplasmic transport receptors exportin 5in mammals and MSN5 in yeast. Consistent with a potential role in nucleocytoplasmic transport, we found that HST interacts with RAN1 in a yeast two-hybrid assay and that a HST-GUS fusion protein is located at the periphery of the nucleus. HST is one of at least 17 members of the importin-βfamily in Arabidopsis and is the first member of this family shown to have an essential function in plants. The hst loss-of-function phenotype suggests that this protein regulates the nucleocytoplasmic transport of molecules involved in several different morphogenetic pathways, as well as molecules generally required for root and shoot growth.
Leaf damage is known to adversely affect reproductive output through the female (fruit and seed) function, but little is known about the effects of leaf damage on the male function of plants. This study simulates the timing, location, and pattern of natural herbivory by diabroticite beetles and shows that leaf damage reduces male reproductive success in Cucurbita texana. Partially defoliated branches of C. texana produced significantly fewer staminate flowers and fewer pollen grains per flower than undamaged branches on the same plant. Moreover, pollen from staminate flowers on partially defoliated plants was less likely to sire seeds than pollen from undamaged plants when deposited onto a stigma with pollen from a tester line, indicating that leaf damage not only decreases pollen production but also adversely affects pollen performance.
During its development, a plant shoot progresses from a juvenile to an adult phase of vegetative growth and from a reproductively incompetent to a reproductively competent state. In Arabidopsis, loss-of-function mutations in SQUINT (SQN) reduced the number of juvenile leaves and had subtle effects on inflorescence morphology but had no effect on flowering time or on reproductive competence. SQN encodes the Arabidopsis homolog of cyclophilin 40 (CyP40), a protein found in association with the Hsp90 chaperone complex in yeast, mammals, and plants. Thus, in Arabidopsis, CyP40 is specifically required for the vegetative but not the reproductive maturation of the shoot.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.