The 2018 rift eruption and summit collapse of Kilauea Volcano.

In 2018, Kilauea Volcano experienced its largest lower East Rift Zone (LERZ) eruption and caldera collapse in at least 200 years. After collapse of the Pu'u 'O'o vent on 30 April, magma propagated downrift. Eruptive fissures opened in the LERZ on 3 May, eventually extending ~6.8 kilometers. A 4 May earthquake [moment magnitude (M w) 6.9] produced ~5 meters of fault slip. Lava erupted at rates exceeding 100 cubic meters per second, eventually covering 35.5 square kilometers. The summit magma system partially drained, producing minor explosions and near-daily collapses releasing energy equivalent to M w 4.7 to 5.4 earthquakes. Activity declined rapidly on 4 August. Summit collapse and lava flow volume estimates are roughly equivalent-about 0.8 cubic kilometers. Careful historical observation and monitoring of Kilauea enabled successful forecasting of hazardous events.

First Report of Sclerotinia minor Infecting Ipomoea hederacea and I. coccinea in Texas.

Sclerotinia blight, caused by the soilborne fungus Sclerotinia minor Jagger, is a major disease of peanut (Arachis hypogaea L.) in parts of west Texas. Previous reports have indicated that annual weed species may serve as collateral hosts for S. minor (2). Several Ipomoea spp. are commonly found in peanut fields throughout the region. In September of 2007, Ipomoea hederacea and I. coccinea plants with bleached, shredded stems, and signs of black sclerotia were collected from a field known to be infested with S. minor. Symptomatic stem sections were rinsed in tap water, surface disinfested in 0.5% sodium hypochlorite for 1 min, air dried, and plated on potato dextrose agar (PDA). Pure cultures of S. minor consisting of white, fluffy mycelia and small (<2 mm), black, irregular sclerotia were consistently recovered. Pathogenicity tests were conducted by wound-inoculating healthy I. hederacea and I. coccinea transplants (n = 3) with agar plugs obtained from the edges of actively growing S. minor cultures. Plants were incubated in a dew chamber at 20°C and 95% relative humidity for 5 days. Plants inoculated with sterile PDA plugs served as controls (n = 3). A similar test was conducted using the susceptible peanut cultivar Flavorunner 458. Characteristic symptoms of Sclerotinia blight (3) were observed on all inoculated weed and peanut plants; whereas, the controls remained healthy. Pathogenicity tests were repeated with similar results. Cultures of S. minor were obtained from all symptomatic tissues, fulfilling Koch's postulates. These results indicate that I. hederacea and I. coccinea are additional hosts of S. minor and that sclerotia produced on infected plants can significantly augment soil inoculum. S. minor has been observed to infect I. batatas seedlings in New Jersey (1); however, this to our knowledge is the first report of S. minor infecting Ipomoea spp. in Texas. Therefore, weed management should inevitability be a part of disease management strategies for the control of Sclerotinia blight in peanut. References: (1) Anonymous. Index of Plant Diseases in the United States. USDA Handb. No. 165, 1960. (2) J. E. Hollowell et al. Plant Dis. 87:197, 2003. (3) D. M. Porter and H. A. Melouk. Sclerotinia blight. Page 34 in: Compendium of Peanut Diseases. 2nd ed. N. Kokalis-Burelle et al., eds. The American Phytopathologicial Society, St. Paul, MN, 1997.

Root Rot by Rhizoctonia solani on Ambrosia grayi in Texas.

Ambrosia grayi (A. Nelson) Shinners is a pernicious perennial weed that infests over 200,000 ha of cotton in Texas and New Mexico. It reproduces primarily by rhizomes, which are found up to 3 m deep in the soil. With the exception of Roundup Ultra on Roundup-ready cotton, no herbicides can be applied in-season to control this weed without injuring cotton. A search was conducted for soilborne pathogens as potential biocontrol agents by surveying cotton fields and small lakes for A. grayi plants with root lesions. Roots were washed with running water for 2 min and segments of root lesions were placed on water agar (1.5%) with hyphae of emerging fungi transferred to potato dextrose agar (PDA). Eighty isolates of fungi were collected; most were Fusarium spp. or Rhizoctonia solani. Replicated experiments with isolates were conducted. Each isolate was grown on PDA and then 1/4 of the media in a petri plate (12.6 cm2) was mixed with 450 cm3 autoclaved soil and placed in a styrofoam cup. A piece of rhizome (3 to 5 cm in length) was placed 5 cm below the soil surface in the infested cup. Roots with necrosis were plated on PDA to recover fungi, which were grown in pure culture and used to reinfest soil. Significant disease (in repeated tests) was caused by two isolates of R. solani, compared with the noninfested check, as indicated by a reduction in number of emerging plants per pot, increase in root necrosis, and decrease in fresh and dried leaf weight. Roots growing from the infected rhizomes were discolored and rotted without distinct lesions. Both of these isolates were identified as AG4 by anastomosis with tester ATCC #46134 by the cellophane technique (1). Reference: (1) D. E. Carling et al. Phytopathology 77:1609, 1987.

Effects of Acetyl-Coenzyme A Carboxylase Inhibitors on Root Cell Transmembrane Electric Potentials in Graminicide-Tolerant and -Susceptible Corn (Zea mays L.).

Herbicidal activity of aryloxyphenoxypropionate and cyclohexanedione herbicides (graminicides) has been proposed to involve two mechanisms: inhibition of acetyl-coenzyme A carboxylase (ACCase) and depolarization of cell membrane potential. We examined the effect of aryloxyphenoxypropionates (diclofop and haloxyfop) and cyclohexanediones (sethoxydim and clethodim) on root cortical cell membrane potential of graminicide-susceptible and -tolerant corn (Zea mays L.) lines. The graminicide-tolerant corn line contained a herbicide-insensitive form of ACCase. The effect of the herbicides on membrane potential was similar in both corn lines. At a concentration of 50 [mu]M, the cyclohexanediones had little or no effect on the membrane potential of root cells. At pH 6, 50 [mu]M diclofop, but not haloxyfop, depolarized membrane potential, whereas both herbicides (50 [mu]M) dramatically depolarized membrane potential at pH 5. Repolarization of membrane potential after removal of haloxyfop and diclofop from the treatment solution was incomplete at pH 5. However, at pH 6 nearly complete repolarization of membrane potential occurred after removal of diclofop. In graminicide-susceptible corn, root growth was significantly inhibited by a 24-h exposure to 1 [mu]M haloxyfop or sethoxydim, but cell membrane potential was unaffected. In gramincide-tolerant corn, sethoxydim treatment (1 [mu]M, 48 h) had no effect on root growth, whereas haloxyfop (1 [mu]M, 48 h) inhibited root growth by 78%. However, membrane potential was the same in roots treated with 1 [mu]M haloxyfop or sethoxydim. The results of this study indicate that graminicide tolerance in the corn line used in this investigation is not related to an altered response at the cell membrane level as has been demonstrated with other resistant species.

Allelic mutations in acetyl-coenzyme A carboxylase confer herbicide tolerance in maize.

The genetic relationship between acetyl-coenzyme A carboxylase (ACCase; EC 6.4.1.2.) activity and herbicide tolerance was determined for five maize (Zea mays L.) mutants regenerated from tissue cultures selected for tolerance to the ACCase-inhibiting herbicides, sethoxydim and haloxyfop. Herbicide tolerance in each mutant was inherited as a partially dominant, nuclear mutation. Allelism tests indicated that the five mutations were allelic. Three distinguishable herbicide tolerance phenotypes were differentiated among the five mutants. Seedling tolerance to herbicide treatments cosegregated with reduced inhibition of seedling leaf ACCase activity by sethoxydim and haloxyfop demonstrating that alterations of ACCase conferred herbicide tolerance. Therefore, we propose that at least three, and possible five, new alleles of the maize ACCase structural gene (Acc1) were identified based on their differential response to sethoxydim and haloxyfop. The group represented by Acc1-S1, Acc1-S2 and Acc1-S3 alleles, which had similar phenotypes, exhibited tolerance to high rates of sethoxydim and haloxyfop. The Acc1-H1 allele lacked sethoxydim tolerance but was tolerant to haloxyfop, whereas the Acc1-H2 allele had intermediate tolerance to sethoxydim but was tolerant to haloxyfop. Differences in tolerance to the two herbicides among mutants homozygous for different Acc1 alleles suggested that sites on ACCase that interact with the different herbicides do not completely overlap. These mutations in maize ACCase should prove useful in characterization of the regulatory role of ACCase in fatty acid biosynthesis and in development of herbicide-tolerant maize germplasm.