Significance The Songpan-Ganzi terrane lies in the central-east of the Tibetan Plateau, which was considered a stable block in some tectonic models. Its deformation mode is of crucial importance for ...understanding the evolutionary history and seismic hazard of the plateau. The recent Maduo earthquake occurred inside the terrane. We resolve a bilateral rupture process with distinct super- and subshear rupture modes for this event. We also find that pervasive folding structures that are aligned by shear deformation in the current Songpan-Ganzi terrane are responsible for the seismic wave anisotropy and shear strain orientation in its upper crust. Its deformation mode can be classified as distributed simple shear, which receives shear loads from side walls and produces internal earthquakes.
Abstract
Fumarylacetoacetate hydrolase (FAH) catalyzes the final step of Tyrosine (Tyr) degradation pathway essential to animals and the deficiency of FAH causes an inborn lethal disease. In plants, ...a role of this pathway was unknown until we found that mutation of
Short-day Sensitive Cell Death1
(
SSCD1
), encoding
Arabidopsis
FAH, results in cell death under short day. Phenylalanine (Phe) could be converted to Tyr and then degraded in both animals and plants. Phe ingestion in animals worsens the disease caused by FAH defect. However, in this study we found that Phe represses cell death caused by FAH defect in plants. Phe treatment promoted chlorophyll biosynthesis and suppressed the up-regulation of reactive oxygen species marker genes in the
sscd1
mutant. Furthermore, the repression of
sscd1
cell death by Phe could be reduced by α-aminooxi-β-phenylpropionic acid but increased by methyl jasmonate, which inhibits or activates Phe ammonia-lyase catalyzing the first step of phenylpropanoid pathway, respectively. In addition, we found that jasmonate signaling up-regulates
Phe ammonia-lyase 1
and mediates the methyl jasmonate enhanced repression of
sscd1
cell death by Phe. These results uncovered the relation between chlorophyll biosynthesis, phenylpropanoid pathway and jasmonate signaling in regulating the cell death resulting from loss of FAH in plants.
•Innovative joint inversion techniques resolve complementary co-seismic slip and afterslip distributions.•Mainshock triggering is likely dominated by a foreshock cascade mechanism.•Early afterslip ...shows distinct seismically or aseismically dominated behavior on orthogonal faults.•Co-seismic stress changes cause afterslip migration on the SW trending fault.
Cascade-up and/or slow-slip processes are commonly believed to control interactions between foreshocks, mainshocks and aftershocks, but their relative contributions remain poorly resolved. Discrimination between these processes will shed light on the understanding of earthquake physics, which requires exceptional observations of earthquake sequences. The well-recorded July 2019 Ridgecrest, California foreshock-mainshock-aftershock earthquake sequence provides such an opportunity. We perform simultaneous inversion of the July 4th MW 6.4 foreshock and July 5th MW 7.1 mainshock kinematic rupture models using SAR, strong motion, and GPS data. We also invert for afterslip models following the MW 6.4 foreshock and the mainshock, respectively, by developing an inversion method that utilizes strainmeter, SAR and daily GPS time series. The inversion results show that the overall sequence involves no less than six fault segments, which include a main northwest-trending fault and secondary faults with sub-parallel and orthogonal geometry to the main fault. Co-seismic slip and afterslip have complementary patterns on the faults. During the early post-seismic period following the MW 6.4 foreshock and the mainshock, moment release on the southwest-trending fault is dominated by aseismic slip, in contrast to the predominantly seismic slip on the northwest-trending fault. The mainshock appears to be triggered by a cascade migration of foreshocks on a northwest-trending fault. Slip on the southwest-trending fault migrates from the fault junction at the northeast end (following the MW 6.4 foreshock) to the southwest end (following the mainshock) during the afterslip interval. The dual-mode (seismic versus aseismic) slip phenomena appear to be driven by co-seismic stress changes produced by the major events.
Some plant and animal pathogens can manipulate their hosts to cause them to release odors that are attractive to the pathogens＇ arthropod vectors. However, the molecular mechanism underlying this ...process is largely unexplored, and the specific effectors the pathogens employ as well as the pathways within the hosts they target are currently unknown. Here we reveal that the aphid-borne cucumber mosaic virus （CMV） employs its 2b protein, a well-charac- terized viral suppressor of host RNA interference （VSR）, to target the host＇s jasmonate （JA） hormone pathway, thus acting as a viral inducer of host attractiveness to insect vectors （VIA）. 2b inhibits JA signaling by directly interacting with and repressing JA-induced degradation of host jasmonate ZIM-domain proteins, instead of using its VSR activ- ity. Our findings identify a previously defined VSR protein as a VIA and uncover a molecular mechanism CMV uses to manipulate host＇s attractiveness to insect vectors by targeting host hormone signaling.
The seismic, geodetic, and tsunami observations are utilized to investigate the October 30th 2020 Samos, Greece earthquake. We adopt back projection (BP) and multi-point source (MPS) techniques to ...determine the rupture directivity and focal mechanism change of this event. Both methods reveal a unilateral rupture propagation to the west of the epicenter, and also resolve a changed focal mechanism. We use a two-segment-faults geometry to parameterize the fault model with strikes at 283° for the east segment and 250° for the west respectively, and conduct a finite fault inversion (FFI) combining seismic and geodetic observations. The kinematics results indicate the whole rupture process lasts about 25 s, yielding a total seismic moment of 3.16×1019 Nm (Mw = 6.9) with a peak moment rate reaching 3.1×1018 Nm/s around 10 s. The rupture is composed of two asperities separated by the junction of two fault planes. The main slip area, with maximum amplitude reaching three meters, distributes at a shallow depth and displays a complementary pattern with aftershocks. The slip in the first six seconds is dominated by a pure normal faulting mechanism, while the following rupture includes an additional strike-slip component. The change of focal mechanism reflects the tectonic transition from dilatation to lateral shearing, which is also evident in the aftershock mechanisms. The synthetic tsunami waves also well fit three tidal gauge observations. The coseismic Coulomb stress is calculated to analyze the relationship between the mainshock and aftershock evolution. The mechanism combination of two rupture epochs reflects the combination of shear and dilatational stress status and complicated fault system of the Samos source area.
•Segmented rupture of the 2020 Mw 6.9 Samos earthquake is revealed by BP and MPS techniques.•The slip model of the event is constrained by multiple observations.•Tsunami wave simulation over the Agean Sea is performed and validated by tidal gauge observations.
Summary
Fumarylacetoacetate hydrolase (FAH) catalyses the final step of the tyrosine degradation pathway, which is essential to animals but was of unknown importance in plants until we found that ...mutation of Short‐day Sensitive Cell Death1 (SSCD1), encoding Arabidopsis FAH, results in cell death under short‐day conditions. The sscd1 mutant accumulates succinylacetone (SUAC), an abnormal metabolite caused by loss of FAH. Succinylacetone is an inhibitor of δ‐aminolevulinic acid (ALA) dehydratase (ALAD), which is involved in chlorophyll (Chl) biosynthesis. In this study, we investigated whether sscd1 cell death is mediated by Chl biosynthesis and found that ALAD activity is repressed in sscd1 and that protochlorophyllide (Pchlide), an intermediate of Chl biosynthesis, accumulates at lower levels in etiolated sscd1 seedlings. However, it was interesting that Pchlide in sscd1 might increase after transfer from light to dark and that HEMA1 and CHLH are upregulated in the light–dark transition before Pchlide levels increased. Upon re‐illumination after Pchlide levels had increased, reactive oxygen species marker genes, including singlet oxygen‐induced genes, are upregulated, and the sscd1 cell death phenotype appears. In addition, Arabidopsis WT seedlings treated with SUAC mimic sscd1 in decline of ALAD activity and accumulation of Pchlide as well as cell death. These results demonstrate that increase in Pchlide causes cell death in sscd1 upon re‐illumination and suggest that a decline in the Pchlide pool due to inhibition of ALAD activity by SUAC impairs the repression of ALA synthesis from the light–dark transition by feedback control, resulting in activation of the Chl biosynthesis pathway and accumulation of Pchlide in the dark.
Significance Statement
The role of the tyrosine degradation pathway in plants is not well understood. This study revealed a relation between the Tyr degradation pathway and the Chl biosynthetic pathway in mediating sscd1 cell death, which provides insight into the biological function of the Tyr degradation pathway in plants and the regulation of the Chl biosynthesis pathway and cell death.
Fumarylacetoacetate hydrolase (FAH) catalyzes the final step in Tyr degradation pathway essential to animals but not well understood in plants. Previously, we found that mutation of SSCD1 encoding ...Arabidopsis FAH causes cell death under short day, which uncovered an important role of Tyr degradation pathway in plants. Since phytohormones salicylic acid (SA) and jasmonate (JA) are involved in programmed cell death, in this study, we investigated whether sscd1 cell death is related to SA and JA, and found that (1) it is accompanied by up-regulation of JA- and SA-inducible genes as well as accumulation of JA but not SA; (2) it is repressed by breakdown of JA signaling but not SA signaling; (3) the up-regulation of reactive oxygen species marker genes in sscd1 is repressed by breakdown of JA signaling; (4) treatment of wild-type Arabidopsis with succinylacetone, an abnormal metabolite caused by loss of FAH, induces expression of JA-inducible genes whereas treatment with JA induces expression of some Tyr degradation genes with dependence of JA signaling. These results demonstrated that cell death resulted from loss of FAH in Arabidopsis is related to JA but not SA, and suggested that JA signaling positively regulates sscd1 cell death by up-regulating Tyr degradation.
Main conclusion
The rice
OsFAH
gene functions identically to that of
Arabidopsis SSCD1
encoding FAH. Loss of
OsFAH
causes rice sterility.
Fumarylacetoacetate hydrolase (FAH) is the last enzyme in the ...tyrosine (Tyr) degradation pathway that is crucial for animals. By genetic analysis of the mutant of
Short-day Sensitive Cell Death 1
gene encoding
Arabidopsis
FAH, we first found the pathway also plays a critical role in plants (Han et al., Plant Physiol 162:1956–1964, 2013). To further understand the role of the Tyr degradation pathway in plants, we investigated a biological function of the rice FAH. Firstly, the cDNA of rice FAH gene (
OsFAH
) was cloned and confirmed to be able to rescue the
Arabidopsis
Short-day Sensitive Cell Death 1
mutant defective in the FAH. Then, we identified the
OsFAH
T-DNA insertion mutant and generated the
OsFAH
RNA interference lines, and found that loss of
OsFAH
results in rice sterility. Furthermore, we analyzed expression of the
OsFAH
gene in roots, stems, leaves and young panicles at booting stage of rice and found that its transcript level was highest in young panicles and lowest in roots. In addition, the expression analysis of β-glucuronidase driven by
OsFAH
promoter in transgenic
Arabidopsis
showed that the
OsFAH
promoter was highly active in aerial tissues in vegetative stage, and sepals, filaments and stigma in reproductive stage. These results suggested that FAH plays an important role in rice fertility.
Jasmonate （JA） regulates plant development, mediates defense responses, and induces anthocyanin biosynthesis as well. Previously, we isolated the psc1 mutant that partially suppressed coi1 ...insensitivity to JA, and found that brassinosteroid （BR） was involved in JA signaling and negatively regulated JA inhibition of root growth in Arabidopsis. In this study it was shown that JA-induced anthocyanin accumulation was reduced in BR mutants or in wild type treated with brassinazole, an inhibitor of BR biosynthesis, whereas it was induced by an application of exogenous BR. It was also shown that the‘late’anthocyanin biosynthesis genes including DFR, LDOX , and UF3GT, were induced slightly by JA in the BR mutants relative to wild type. Furthermore, the expression level of JA-induced Myb/bHLH transcription factors such as PAP1, PAP2, and GL3, which are components of the WD-repeat/Myb/bHLH transcriptional complexes that mediate the ‘late’ anthocyanin biosynthesis genes, was lower in the BR mutants than that in wild type. These results suggested that BR affects JA-induced anthocyanin accumulation by regulating the ‘late’ anthocyanin biosynthesis genes and this regulation might be mediated by the WD-repeat/Myb/bHLH transcriptional complexes.
The F-box protein CORONATINE INSENSITIVE1 (COl1) plays a central role in jasmonate (JA) signaling and is required for all JA responses in Arabidopsis (Arabidopsis thaliana). To dissect JA signal ...transduction, we isolated the partially suppressing (psc1) mutant, which partially suppressed coil insensitivity to JA inhibition of root growth. The pscl mutant partially restored JA sensitivity in coil-2 background and displayed JA hypersensitivity in wild-type COl1 background. Genetic mapping, sequence analysis, and complementation tests revealed that psc1 is a leaky mutation of DWARF4 (DWF4) that encodes a key enzyme in brassinosteroid (BR) biosynthesis. Physiological analysis showed that an application of exogenous BR eliminated the partial restoration of JA sensitivity by pscl in coi1-2 background and the JA hypersensitivity of psc1 in wild-type COl1 background. Exogenous BR also attenuated JA inhibition of root growth in the wild type. In addition, the expression of DWF4 was inhibited by JA, and this inhibition was dependent on COl1. These results indicate that (1) BR is involved in JA signaling and negatively regulates JA inhibition of root growth, and (2) the DWF4 is down-regulated by JA and is located downstream of COl1 in the JA-signaling pathway.
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