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Fungal susceptibility and early flowering in pennycress (Thlaspi arvense) are conferred by naturally occurring mutations in histone demethylase Jumonji 14

ABSTRACT: Fungal susceptibility and early flowering in pennycress (Thlaspi arvense) are conferred by naturally occurring mutations in histone demethylase Jumonji 14

PROVIDER: PRJNA1251596 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33173936_1.fastq.gz	Fastqsanger.gz
	SRR33173936_2.fastq.gz	Fastqsanger.gz
	SRR33173937_1.fastq.gz	Fastqsanger.gz
	SRR33173937_2.fastq.gz	Fastqsanger.gz
	SRR33173938_1.fastq.gz	Fastqsanger.gz

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Fungal susceptibility and early flowering in pennycress (Thlaspi arvense) are conferred by naturally occurring mutations in histone demethylase Jumonji 14

Project description:Pennycress (Thlaspi arvense) is a winter oilseed domesticated recently to be incorporated as an intermediate crop between the existing cropping systems of the US Midwest. We show that a natural accession of pennycress, 2032, is more susceptible to the necrotrophic fungal pathogens Sclerotinia sclerotiorum and Alternaria japonica than the reference pennycress accession MN106. A previously identified marker associated with earliness in pennycress was found to be present in in a gene homologous to Arabidopsis Jumonji 14 (JMJ14). It has been reported that AtJMJ14 promotes disease resistance and represses flowering, and greenhouse studies of breeding populations confirmed this phenomenon in pennycress. Plants with the 2032 TaJMJ14 allele were more susceptible to fungi and flowered early. CRISPR-Cas9 editing was used to generate additional TaJMJ14 alleles. A 9 bp deletion in TaJMJ14 showed trends of early flowering and S. sclerotiorum susceptibility, whereas a complete loss-of-function allele led to infertility. We further investigated the transcriptomes of MN106 and 2032 plants in the early stages of S. sclerotiorum and A. japonica infection to identify potential resistance and susceptibility genes. Differences in the expression of pathogen-associated molecular pattern-triggered immunity (PTI)-associated genes led us to discover that 2032 plants have defects in elicitor-triggered oxidative bursts. The transcriptional responses unique to each accession lay a foundation for future gene-editing and breeding approaches to keep the beneficial early flowering phenotype conferred by 2032 but uncouple it from disease susceptibility.

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Project description:Thlaspi arvense (field pennycress) is an emerging oilseed crop closely related to Arabidopsis thaliana. Prior research on oilseed species has demonstrated that seed specific upregulation of WRINKLED1 (WRI1), a key regulator of triacylglycerol (TAG) biosynthesis, can augment seed oil content. This phenomenon extends to the TAG biosynthetic enzyme diglyceride acyltransferase 1 (DGAT1). In this study, we show that stable co-expression of WRI1 and DGAT1 in pennycress during seed development significantly elevates oil content in mature seeds. Utilizing in vitro cultured developing embryos, we thoroughly characterized the alterations in seed composition resulting from WRI1/DGAT1 overexpression, employing a combination of transcriptomic analysis, targeted metabolomics, and metabolic flux analysis.

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Project description:Little is known about the role of the three Jumonji C (JmjC) enzymes in Plasmodium falciparum (Pf). Here, we show that JIB-04 and other established inhibitors of mammalian JmjC histone demethylases kill asexual blood stage parasites and are even more potent at blocking gametocyte development and gamete formation. In late stage parasites, JIB-04 increased levels of trimethylated lysine residues on histones, suggesting the inhibition of P. falciparum Jumonji demethylase activity. These epigenetic defects coincide with deregulation of invasion, cell motor, and sexual development gene programs, including gene targets coregulated by the PfAP2-I transcription factor and chromatin-binding factor, PfBDP1. Mechanistically, we demonstrate that PfJmj3 converts 2-oxoglutarate to succinate in an iron-dependent manner consistent with mammalian Jumonji enzymes, and this catalytic activity is inhibited by JIB-04 and other Jumonji inhibitors. Our pharmacological studies of Jumonji activity in the malaria parasite provide evidence that inhibition of these enzymatic activities is detrimental to the parasite.

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