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The functions of dicot sucrose transporters (SUTs) in apoplastic phloem loading of sucrose are well established; however, whether SUTs similarly function in monocots was unresolved. To address this question, we recently provided genetic evidence that ZmSUT1from maize (Zea mays) is required for efficient phloem loading. sut1-m1mutant plants hyperaccumulate carbohydrates in leaves, are defective in loading sucrose into the phloem, and have altered biomass partitioning. Presumably due to the hyperaccumulation of soluble sugars in leaves, mutations in ZmSUT1lead to downregulation of chlorophyll accumulation, photosynthesis and stomatal conductance. However, because we had identified only a single mutant allele, we were not able to exclude the possibility that the mutant phenotypes were instead caused by a closely linked mutation. Based on a novel aspect of the sut1 mutant phenotype, secretion of a concentrated sugar solution from leaf hydathodes, we identified an additional mutant allele, sut1-m4. This confirms that the mutation of SUT1is responsible for the impairment in phloem loading. In addition, the sut1-m4mutant does not accumulate transcripts, supporting the findings reported previously that the original mutant allele is also a null mutation. Collectively, these data demonstrate that ZmSUT1functions to phloem load sucrose in maize leaves.

The success of a breeding program depends on having adequate diversity in the germplasm. However, as advanced breeding stocks and materials are generated, one casualty is the diversity itself. As a result, breeding programs in many crop species have reached a point of diminishing returns and it is feared that unless new diversity is infused into the breeding germplasm, we face catastrophic reductions in crop productivity if the climate turns adverse. Although some scientists favor transgenic approaches, a “back to nature” approach to genetic diversity may prove faster and more effective. Wild and exotic relatives of crop plants hold a wealth of alleles that, if we can find them, can help break yield barriers and enhance tolerance to stresses. Many approaches, based largely on quantitative trait loci genetics, have been proposed and used for this purpose, but most are either highly laborious or discover relevant variation inefficiently. Here, we propose a gene‐centered approach, dubbed MAGIC (mutant‐assisted gene identification and characterization), that uses Mendelian mutants or other genetic variants in a trait of interest as reporters to identify novel genes and variants for that trait. MAGIC is similar to enhancer–suppressor screens, but rather than relying on variation created in the laboratory, it reveals variation created and refined by nature over millions of years of evolution. This approach could be an effective tool for exploring novel variation and a valuable means to harness natural diversity and define genetic networks.

We reported previously the isolation of a novel cell death-suppressing gene from maize (Zea mays) encoded by the Lls1 (Lethal leaf spot-1) gene. Although the exact metabolic function of LLS1 remains elusive, here we provide insight into mechanisms that underlie the initiation and propagation of cell death associated with lls1 lesions. Our data indicate that lls1 lesions are triggered in response to a cell-damaging event caused by any biotic or abiotic agent or intrinsic metabolic imbalance--as long as the leaf tissue is developmentally competent to develop lls1 lesions. Continued expansion of these lesions, however, depends on the availability of light, with fluence rate being more important than spectral quality. Double-mutant analysis of lls1 with two maize mutants oil-yellow and iojap, both compromised photosynthetically and unable to accumulate normal levels of chlorophyll, indicated that it was the light harvested by the plant that energized lls1 lesion development. Chloroplasts appear to be the key mediators of lls1 cell death; their swelling and distortion occurs before any other changes normally associated with dying cells. In agreement with these results are indications that LLS1 is a chloroplast-localized protein whose transcript was detected only in green tissues. The propagative nature of light-dependent lls1 lesions predicts that cell death associated with these lesions is caused by a mobile agent such as reactive oxidative species. LLS1 may act to prevent reactive oxidative species formation or serve to remove a cell death mediator so as to maintain chloroplast integrity and cell survival.

Prohibitins, stomatins, and a group of plant defense response genes are demonstrated to belong to a novel protein superfamily. This superfamily is bound by similar primary and secondary predicted protein structures and hydropathy profiles. A PROSITE-formatted regular expression was generated that is highly predictive for identifying members of this superfamily using PHI-BLAST. The superfamily is named PID (proliferation,ion, and death) because prohibitins are involved in proliferation and cell cycle control, stomatins are involved in ion channel regulation, and the plant defense-related genes are involved in cell death. The plant defense gene family is named HIR (hypersensitive induced reaction) because its members are associated with hypersensitive reactions involving cell death and pathogen resistance. For this study, eight novel maize genes were introduced: four closely related to prohibitins (Zm-phb1, Zm-phb2, Zm-phb3, and Zm-phb4), one to stomatins (Zm-stm1), and three to a gene implicated in plant disease responses (Zm-hir1, Zm-hir2, and Zm-hir3). The maize Zm-hir3gene transcript is up-regulated in a disease lesion mimic mutation (Les9), supporting a role in maize defense responses. Members of this gene superfamily are involved in diverse functions, but their structural similarity suggests a conserved molecular mechanism, which we postulate to be ion channel regulation.