ArticleBMC plant biology2022
Chloroplastic pentatricopeptide repeat proteins (PPR) in albino plantlets of Agave angustifolia Haw. reveal unexpected behavior.
Article in BMC plant biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Article
- Updated Progress on Group II Intron Splicing Factors in Plant Chloroplasts.Current issues in molecular biology · 2022Review
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4 authors at 2 institutions in 1 country.
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Abstract
backgroundPentatricopeptide repeat (PPR) proteins play an essential role in the post-transcriptional regulation of genes in plastid genomes. Although important advances have been made in understanding the functions of these genes, there is little information available on chloroplastic PPR genes in non-model plants and less in plants without chloroplasts. In the present study, a comprehensive and multifactorial bioinformatic strategy was applied to search for putative PPR genes in the foliar and meristematic tissues of green and albino plantlets of the non-model plant Agave angustifolia Haw.
resultsA total of 1581 PPR transcripts were identified, of which 282 were chloroplastic. Leaf tissue in the albino plantlets showed the highest levels of expression of chloroplastic PPRs. The search for hypothetical targets of 12 PPR sequences in the chloroplast genes of A. angustifolia revealed their action on transcripts related to ribosomes and translation, photosystems, ATP synthase, plastid-encoded RNA polymerase and RuBisCO.
conclusionsOur results suggest that the expression of PPR genes depends on the state of cell differentiation and plastid development. In the case of the albino leaf tissue, which lacks functional chloroplasts, it is possible that anterograde and retrograde signaling networks are severely compromised, leading to a compensatory anterograde response characterized by an increase in the expression of PPR genes.
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