Control of sexuality by the sk1-encoded UDP-glycosyltransferase of maize.

Sex determination in maize involves the production of staminate and pistillate florets from an initially bisexual floral meristem. Pistil elimination in staminate florets requires jasmonic acid signaling, and functional pistils are protected by the action of the silkless 1 (sk1) gene. The sk1 gene was identified and found to encode a previously uncharacterized family 1 uridine diphosphate glycosyltransferase that localized to the plant peroxisomes. Constitutive expression of an sk1 transgene protected all pistils in the plant, causing complete feminization, a gain-of-function phenotype that operates by blocking the accumulation of jasmonates. The segregation of an sk1 transgene was used to effectively control the production of pistillate and staminate inflorescences in maize plants.

Identification of the maize gravitropism gene lazy plant1 by a transposon-tagging genome resequencing strategy.

Since their initial discovery, transposons have been widely used as mutagens for forward and reverse genetic screens in a range of organisms. The problems of high copy number and sequence divergence among related transposons have often limited the efficiency at which tagged genes can be identified. A method was developed to identity the locations of Mutator (Mu) transposons in the Zea mays genome using a simple enrichment method combined with genome resequencing to identify transposon junction fragments. The sequencing library was prepared from genomic DNA by digesting with a restriction enzyme that cuts within a perfectly conserved motif of the Mu terminal inverted repeats (TIR). Paired-end reads containing Mu TIR sequences were computationally identified and chromosomal sequences flanking the transposon were mapped to the maize reference genome. This method has been used to identify Mu insertions in a number of alleles and to isolate the previously unidentified lazy plant1 (la1) gene. The la1 gene is required for the negatively gravitropic response of shoots and mutant plants lack the ability to sense gravity. Using bioinformatic and fluorescence microscopy approaches, we show that the la1 gene encodes a cell membrane and nuclear localized protein. Our Mu-Taq method is readily adaptable to identify the genomic locations of any insertion of a known sequence in any organism using any sequencing platform.

What can plant autophagy do for an innate immune response?

Autophagy plays an established role in the execution of senescence, starvation, and stress responses in plants. More recently, an emerging role for autophagy has been discovered during the plant innate immune response. Recent papers have shown autophagy to restrict, and conversely, to also promote programmed cell death (PCD) at the site of pathogen infection. These initial studies have piqued our excitement, but they have also revealed gaps in our understanding of plant autophagy regulation, in our ability to monitor autophagy in plant cells, and in our ability to manipulate autophagic activity. In this review, we present the most pressing questions now facing the field of plant autophagy in general, with specific focus on autophagy as it occurs during a plant-pathogen interaction. To begin to answer these questions, we place recent findings in the context of studies of autophagy and immunity in other systems, and in the context of the mammalian immune response in particular.

Special delivery for MHC II via autophagy.

In this issue of Immunity, Blanchet et al. (2010) report that human immunodeficiency virus-1 inhibits macroautophagy in dendritic cells, attenuating MHC II presentation. Lee et al. (2010) previously revealed the requirement of autophagic machinery for MHC II presentation of herpes viral antigens.

Something old, something new: plant innate immunity and autophagy.

Autophagy performs a variety of established functions during plant growth and development. Recently, autophagy has been further implicated in the regulation of programmed cell death induced during the plant innate immune response. In this chapter we describe specific mechanisms through which autophagy may contribute to a successful defense against pathogen invasion. Accumulating evidence shows that the plant immune system utilizes the chloroplasts as primary sites for the regulation of cell death programs. Viruses also appear to utilize the chloroplast as a site of replication and accumulation, potentially inactivating chloroplast defense signaling in the process. Autophagy-like mechanisms have been observed to target the chloroplast, which we refer to as "chlorophagy," potentially targeting invasive viruses for degradation or regulating chloroplast-based signaling during the immune response. We hypothesize that chlorophagy is significant for the execution of plant immune defenses, during both basal and effector-triggered immunity.

Autophagy and plant innate immunity: Defense through degradation.

Autophagy is a process of bulk degradation and nutrient sequestration that occurs in all eukaryotes. In plants, autophagy is activated during development, environmental stress, starvation, and senescence. Recent evidence suggests that autophagy is also necessary for the proper regulation of hypersensitive response programmed cell death (HR-PCD) during the plant innate immune response. We review autophagy in plants with emphasis on the role of autophagy during innate immunity. We hypothesize a role for autophagy in the degradation of pro-death signals during HR-PCD, with specific focus on reactive oxygen species and their sources. We propose that the plant chloroplasts are an important source of pro-death signals during HR-PCD, and that the chloroplast itself may be targeted for autophagosomal degradation by a process called chlorophagy.