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Johal, G. S.

Publications and source records attributed to Johal, G. S..

6 recordsLinked to original sources
bioRxiv2022

Genome-wide association identifies impacts of chlorophyll levels on reproductive maturity and architecture in maize

The semi-dominant mutant allele Oy1-N1989 encodes a dominant-negative subunit I of Mg-Chelatase that catalyzes the first committed step of chlorophyll biosynthesis. Analyses of mutant F1 hybrids from crosses of Oy1-N1989 to diverse maize lines identified a natural variant at oil yellow1 as major modifier of chlorophyll content. Chlorophyll reduction increased the time to reproductive maturity, decreased stalk width, and had complex effects on plant height. We explored these effects by genome wide association studies of F1 hybrids crosses of Oy1-N1989 to a maize diversity panel. The delay in reproductive maturity in Oy1-N1989/+ mutants neither altered the vegetative-to-adult phase change nor total leaf number but did slow the rate of organ emergence from the whorl. In addition to the allele at oy1, analysis of tetrapyrrole, heme, and chlorophyll biosynthesis pathway genes identified multiple modifiers of mutant traits. Consistent with organ emergence, rather than a developmental delay, affecting the reproductive delay of Oy1-N1989/+ mutants, known flowering time regulators did not affect variation in the reproductive delay affected by chlorophyll loss. Plant height showed a complex relationship with chlorophyll. The Oy1-N1989/+ mutant F1 plants with a modest reduction in chlorophyll were taller than their wildtype siblings, but F1 plants with dramatically decreased chlorophyll were shorter than their wildtype siblings. Perturbations in the biosynthesis of the phytochrome chromophore increased plant height in wild-type plants but dramatically reduced plant height and chlorophyll contents of Oy1-N1989/+ mutants. The mechanism by which the interaction between chlorophyll and bilin affects height and chlorophyll remains to be explored. One sentence summaryChlorophyll reduction in maize delays reproductive maturity by altering growth and not development, and depending on the reduction can either increase or decrease plant height.

plant biology↗
bioRxiv2022

Disruption of Zea mays isochorismate synthase1 decreases PHENYLALANINE AMMONIA LYASE activity and suppresses hypersensitive response-induced metabolism

ISOCHORISMATE SYNTHASE (ICS) catalyzes the isomerization of chorismate to isochorismate, an essential precursor in the biosynthesis of the Photosystem I electron carrier phylloquinone and of one of two pathways for the biosynthesis of the defense response hormone salicylic acid (SA). We characterized a Zea mays ics1 mutant for impacts on metabolism, photosynthesis, and immune signaling. Phylloquinone was reduced in the mutant resulting in low electron transfer rates and high electron backflow rates. SA accumulation induced by autoactive alleles of the nucleotide-binding leucine-rich repeat (NLR) gene Resistance to Puccinia sorgi1 (Rp1) required ics1. Induced accumulation of SA was not required for lesion formation by the autoactive Rp1-D21#4 allele. Metabolomic analyses and SA supplementation of Rp1-D21#4 mutants, ics1-1 mutants and Rp1-D21#4; ics1-1 double mutants demonstrated that most hypersensitive response-induced metabolism required ics1 but this was independent of SA accumulation. Both the PAL and ICS pathways contributed to SA biosynthesis in maize as labeled phenylalanine was incorporated into SA glucoside. Maize ics1-1 mutants had low PHENYLALANINE AMMONIA LYASE activity, accumulated phenylalanine, and decreased abundance of phenylalanine derived metabolites. This demonstrates that the ICS and PAL pathways interact by a yet unknown mechanism complicating the interpretation of SA biosynthesis in plants from genetics alone.

plant biology↗
bioRxiv2020

Mutation of the nuclear pore complex component, aladin1, disrupts asymmetric cell division in Zea mays (maize)

The nuclear pore complex (NPC) regulates the movement of macromolecules between the nucleus and cytoplasm. Dysfunction of many components of the NPC results in human genetic diseases, including triple A syndrome (AAAS) as a result of mutations in ALADIN. Here we report a nonsense mutation in the maize ortholog, aladin1 (ali1-1), at the orthologous amino acid residue of an AAAS allele from humans, alters plant stature, tassel architecture, and asymmetric divisions of subsidiary mother cells (SMCs). Crosses with the stronger nonsense allele ali1-2 identified complex allele interactions for plant height and aberrant SMC division. RNA-seq analysis of the ali1-1 mutant identified compensatory transcript accumulation for other NPC components as well as gene expression consequences consistent with conservation of ALADIN1 functions between humans and maize. These findings demonstrate that ALADIN1 is necessary for normal plant development, shoot architecture, and asymmetric cell division in maize.

genetics↗
bioRxiv2018

Adult Plant Resistance in Maize to Northern Leaf Spot Is a Feature of Partial Loss-of-function Alleles of Hm1

Adult plant resistance (APR) is an enigmatic phenomenon in which resistance genes are ineffective in protecting seedlings from disease but confer robust resistance at maturity. Maize has multiple cases in which genes confer APR to northern leaf spot, a lethal disease caused by Cochliobolus carbonum race 1 (CCR1). The first identified case of APR in maize is encoded by a hypomorphic allele, Hm1A, at the hm1 locus. In contrast, wild type alleles of hm1 provide complete protection at all developmental stages and in every part of the maize plant. Hm1 encodes an NADPH-dependent reductase, which inactivates HC-toxin, a key virulence effector of CCR1. Cloning and characterization of Hm1A ruled out differential transcription or translation for its APR phenotype and identified an amino acid substitution that reduced HC-toxin reductase (HCTR) activity. The possibility of a causal relationship between the weak nature of Hm1A and its APR phenotype was confirmed by the generation of two new APR alleles of Hm1 by mutagenesis. The HCTRs encoded by these new APR alleles had undergone relatively conservative missense changes that partially reduced their enzymatic activity similar to HM1A. No difference in accumulation of HCTR was observed between adult and juvenile plants, suggesting that the susceptibility of seedlings derives from a greater need for HCTR activity, not reduced accumulation of the gene product. Conditions and treatments that altered the photosynthetic output of the host had a dramatic effect on resistance imparted by the APR alleles, demonstrating a link between the energetic or metabolic status of the host and disease resistance affected by HC-toxin catabolism by the APR alleles of HCTR.\n\nAUTHOR SUMMARYAdult plant resistance (APR) is a phenomenon in which disease resistance genes are able to confer resistance at the adult stages of the plant but somehow fail to do so at the seedling stages. Despite the widespread occurrence of APR in various plant diseases, the mechanism underlying this trait remains obscure. It is not due to the differential transcription of these genes, and here we show that it is also not due to the differential translation or activity of the APR alleles of the maize hm1 gene at different stages of development. Using a combination of molecular genetics, biochemistry and physiology, we present multiple lines of evidence that demonstrate that APR is a feature or symptom of weak forms of resistance. While the mature parts of the plant are metabolically robust enough to manifest resistance, seedling tissues are not, leaving them vulnerable to disease. Growth conditions that compromise the photosynthetic output of the plant further deteriorate the ability of the seedlings to protect themselves from pathogens.\n\nOne sentence summaryCharacterization of adult plant resistance in the maize-CCR1 pathosystem reveals a causal link between weak resistance and APR.

pathology↗
bioRxiv2017

A Very Oil Yellow1 modifier of the Oil Yellow1-N1989 allele uncovers a cryptic phenotypic impact of cis-regulatory variation in maize

Forward genetics determines the function of genes underlying trait variation by identifying the change in DNA responsible for changes in phenotype. Detecting phenotypically-relevant variation outside protein coding sequences and distinguishing this from neutral variants is not trivial; partly because the mechanisms by which DNA polymorphisms in the intergenic regions affect gene regulation are poorly understood. Here we utilized a dominant genetic marker with a convenient phenotype to investigate the effect of cis and trans-acting regulatory variation. We performed a forward genetic screen for natural variation that suppress or enhance the semi-dominant mutant allele Oy1-N1989, encoding the magnesium chelatase subunit I of maize. This mutant permits rapid phenotyping of leaf color as a reporter for chlorophyll accumulation, and mapping of natural variation in maize affecting chlorophyll metabolism. We identified a single modifier locus segregating between B73 and Mo17 that was linked to the reporter gene itself, which we call very oil yellow1. Based on the variation in OY1 transcript abundance and genome-wide association data, vey1 is predicted to consist of multiple cis-acting regulatory sequence polymorphisms encoded at the wild-type oy1 alleles. The vey1 allele appears to be a common polymorphism in the maize germplasm that alters the expression level of a key gene in chlorophyll biosynthesis. These vey1 alleles have no discernable impact on leaf chlorophyll in the absence of the Oy1-N1989 reporter. Thus, use of a mutant as a simple and efficient reporter for magnesium chelatase activity resulted in the detection of expression-level polymorphisms not readily visible in the laboratory.

genetics↗