Plant vacuole sRNAs
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB41301 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4833320.fastq.gz | Fastqsanger.gz | |||
| ERR4833321.fastq.gz | Fastqsanger.gz | |||
| ERR4833322.fastq.gz | Fastqsanger.gz | |||
| ERR4833323.fastq.gz | Fastqsanger.gz | |||
| ERR4833324.fastq.gz | Fastqsanger.gz |
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Project description:Plants balance their conflicting requirements for growth and stress tolerance via sophisticated pathways and unique genes that control responses to the external environment. We have identified a novel plant-specific gene, COST1(Constitutively Stressed 1), that affects plant growth and negatively regulates drought resistance by manipulating the autophagy pathway. An Arabidopsis cost1 mutant has decreased growth and increased drought tolerance, together with constitutive autophagy and increased expression of drought-response genes. The COST1 protein is degraded upon plant dehydration, and this degradation is blocked by treatment with inhibitors of the 26S proteasome or autophagy pathways. The cost1 mutant drought resistance is dependent on an active autophagy pathway, indicating that COST1 acts through manipulation of autophagy. COST1 co-localizes to autophagosomes with the autophagosome marker ATG8e and the autophagy adaptor NBR1, and physically interacts with ATG8e, indicating a pivotal role in direct regulation of autophagy. We propose a model in which COST1 represses autophagy under optimal conditions, thus allowing plant growth. During drought, COST1 is degraded, enabling activation of autophagy and suppressing growth to enhance drought tolerance.
2020-04-16 | GSE113515 | GEO
Project description:Autophagy is essential for plant response to a variety of developmental and environmental factors. However, unlike yeast and animals, only a few autophagy genes in plants are functionally conserved in the biological world. An important question is, how plants form autophagy related functions in evolution? Here, we developed and verified a workflow that identified 997 high-confidence autophagy related genes (ARG) in A.thaliana using multi-group data from nearly 10,000 samples and established a co-network of autophagy containing 3,419 new presumptive connections. Of note, through the genomic analysis of 76 representative plants from lower to higher levels, we found that ARGs were preferentially retained after polyploidization followed by terrestrialization, forming plant-specific autophagy-related functions. In addition, we provide the evolutionary gains and losses of ARGs function in monocotyledons and dicotyledons, and verified two novel genes ml2 and ml5 presumed to be involved in autophagy and leaf senescence. This work provides valuable resources for the study of plant autophagy and highlights that ARGs may selectively promote the success of plant autophagy through polyploidy in the process of evolution.
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Project description:Brassinosteroids (BRs) regulate plant growth, development and stress responses by activating the core transcription factor BRI1-EMS-SUPPRESSOR1 (BES1). The E3 Ubiquitin ligase(s) that modify BES1 for autophagy-mediated degradation remain to be fully defined. In this study, we identified an F-box family E3 ubiquitin ligase termed BES1-ASSOCIATED F-BOX1 (BAF1). BAF1 interacts with and ubiquitinates BES1. Accordingly, BES1 stability and protein levels were reduced in BAF1 overexpression plants but increased in a baf1 loss-of-function mutant and in BAF1-DF (BAF1 with F-box deleted, dominant-negative form) overexpression lines. Selective autophagy of BES1, but not bulk autophagy, was significantly compromised in the baf1 mutant under sucrose starvation. BES1 degradation mediated by BAF1 could be blocked through autophagy but not proteasome inhibitors, suggesting that BAF1 mediates BES1 degradation largely through autophagy. baf1 and BAF1-DF overexpression plants had increased BR-regulated growth but were sensitive to long-term sucrose starvation, while BAF1 overexpression plants had decreased BR-regulated growth but were highly tolerant of sucrose starvation. Our results not only established BAF1 as a novel E3 ubiquitin ligase that targets BES1 for degradation through selective autophagy pathway, but also revealed a mechanism for plants to reduce growth during sucrose starvation by targeting this central growth regulator.
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Project description:Autophagy is a highly conserved pathway responsible for the bulk degradation of cytoplasmic material through the formation of a double-membrane structure known as the autophagosome. However, the precise mechanisms governing the transport of autophagosomes to the vacuole for degradation in plants remain largely elusive. There exists an ongoing debate about whether RAB7, a key regulatory protein, is involved in the plant autophagy pathway. In this study, we demonstrate that upon autophagy induction by BTH treatment, RABG3e, a member of the RAB7 family, exhibits a partial localization with late-stage autophagosomes in Arabidopsis root cells, and its dysfunction leads to the accumulation of enlarged multilayered autophagosomes and a significant reduction in autophagic flux. We also showed that RABG3e is recruited to autophagosomes by its GEF (guanine nucleotide exchange factor) complex, MON1-CCZ1, which is targeted through the interaction between CCZ1 and SH3P2 (SH3 domain-containing protein 2), a plant-specific autophagy regulator. Subsequently, RABG3e recruits the HOPS (homotypic fusion and vacuole protein sorting) complex, which facilitates the recruitment of SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptors) proteins, including SYP21, VTI12, SYP51, and VAMP711, that are essential for the fusion process. Arabidopsis mutants with dysfunction in the autophagosome-vacuole fusion process exhibit accelerated senescence and increased sensitivity to nitrogen starvation. Collectively, our findings provide new insights into the regulation of autophagosome-vacuole fusion in Arabidopsis, highlighting the essential roles of SH3P2-dependent targeting of the CCZ1-MON1-RABG3e module to late-stage autophagosomes as well as the RAB7 effector HOPS and the unique SNARE complex.
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Project description:Members of the fungal genus Armillaria are necrotrophic pathogens with efficient plant biomass-degrading strategies. Armillaria species are some of the largest terrestrial organisms on Earth that cause tremendous losses in diverse ecosystems. Despite their global importance, how Armillaria evolved pathogenicity in a clade of dominantly non-pathogenic wood-degraders (Agaricales) remains elusive. Here, using new genomic data, we show that Armillaria species, in addition to widespread gene duplications and de novo gene origins, appear to have acquired at least 1025 genes via 124 horizontal gene transfer (HGT) events, primarily from Ascomycota donors. Functional and expression data suggest that HGT might have affected plant biomass-degrading and virulence abilities of Armillaria, two pivotal traits in their lifestyle. HGT provides an explanation for their soft-rot like biomass degrading strategy too, which is markedly different from the primarily white rot decay mechanism of related species. Combined multi-species expression data revealed putative virulence factors, extensive regulation of horizontally acquired and wood-decay related genes as well as novel noserved pathogenicity-induced small secreted proteins (PiSSPs). Two PiSSPs induced necrosis in live plants, suggesting they are potential virulence effectors conserved across Armillaria. Overall, this study details how evolution knitted together horizontally and vertically inherited genes in complex adaptive traits, such as plant biomass degradation and pathogenicityin one of the most influential fungal pathogens of temperate forest ecosystems.
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