scholarly journals The Expression of Nuclear Genes Encoding Plastid Ribosomal Proteins Precedes the Expression of Chloroplast Genes during Early Phases of Chloroplast Development

1995 ◽  
Vol 108 (2) ◽  
pp. 685-692 ◽  
Author(s):  
H. Harrak ◽  
T. Lagrange ◽  
C. Bisanz-Seyer ◽  
S. Lerbs-Mache ◽  
R. Mache
Keyword(s):  
Ribosomal Proteins ◽  
Chloroplast Development ◽  
Nuclear Genes ◽  
Chloroplast Genes ◽  
Genes Encoding ◽  
Early Phases

A Tale of Two Genomes: Role of a Chloroplast Signal in Coordinating Nuclear and Plastid Genome Expression

1992 ◽  
Vol 19 (4) ◽  
pp. 387 ◽  
Author(s):  
RE Susek ◽  
J Chory
Keyword(s):  
Chloroplast Development ◽  
Photosynthetic Apparatus ◽  
Signal Transduction Pathway ◽  
Nuclear Genes ◽  
Signal Molecules ◽  
Chloroplast Gene Expression ◽  
Genome Expression ◽  
Coordinate Control ◽  
Genes Encoding

Plant cells coordinately regulate the expression of nuclear and plastid genes that encode components of the photosynthetic apparatus. Nuclear genes that regulate chloroplast development and chloroplast gene expression provide part of this coordinate control. However, there is compelling evidence that information also flows in the opposite direction, from chloroplasts to the nucleus. This hypothesised, second pathway functions to coordinate the expression of nuclear genes encoding components of the photosynthetic apparatus with the functional state of the chloroplast. Here we review the evidence for the signal transduction pathway from the chloroplasts to the nucleus and suggest possible signal molecules.

Motif analysis unveils the possible co-regulation of chloroplast genes and nuclear genes encoding chloroplast proteins

2012 ◽  
Vol 80 (2) ◽  
pp. 177-187
Author(s):  
Ying Wang ◽  
Jun Ding ◽  
Henry Daniell ◽  
Haiyan Hu ◽  
Xiaoman Li
Keyword(s):  
Nuclear Genes ◽  
Chloroplast Genes ◽  
Motif Analysis ◽  
Chloroplast Proteins ◽  
Genes Encoding

Congenital neutropenia

Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 344-350 ◽  
Author(s):  
Christoph Klein
Keyword(s):  
Ribosomal Proteins ◽  
Mitochondrial Proteins ◽  
Phenotypic Traits ◽  
Genetic Defects ◽  
Congenital Neutropenia ◽  
Lysosomal Function ◽  
Genes Encoding ◽  
And Function ◽  
Neutrophil Differentiation ◽  
Remarkable Progress

Abstract Congenital neutropenia comprises a variety of genetically heterogeneous phenotypic traits. Molecular elucidation of the underlying genetic defects has yielded important insights into the physiology of neutrophil differentiation and function. Non-syndromic variants of congenital neutropenia are caused by mutations in ELA2, HAX1, GFI1, or WAS. Syndromic variants of congenital neutropenia may be due to mutations in genes controlling glucose metabolism (SLC37A4, G6PC3) or lysosomal function (LYST, RAB27A, ROBLD3/p14, AP3B1, VPS13B). Furthermore, defects in genes encoding ribosomal proteins (SBDS, RMRP) and mitochondrial proteins (AK2, TAZ) are associated with congenital neutropenia syndromes. Despite remarkable progress in the field, many patients with congenital neutropenia cannot yet definitively be classified by genetic terms. This review addresses diagnostic and therapeutic aspects of congenital neutropenia and covers recent molecular and pathophysiological insights of selected congenital neutropenia syndromes.

The Nuclear Genes for Chloroplast Ribosomal Proteins L11 and L12 in Higher Plants

1993 ◽  
pp. 555-564
Author(s):  
Jürgen Schmidt ◽  
Wolfgang Weglöhner ◽  
Alap R. Subramanian
Keyword(s):  
Ribosomal Proteins ◽  
Higher Plants ◽  
Nuclear Genes

scholarly journals Loss of COX4i1 leads to combined respiratory chain deficiency and impaired mitochondrial proteosynthesis

2020 ◽  
Author(s):  
Čunátová Kristýna ◽  
Pajuelo Reguera David ◽  
Vrbacký Marek ◽  
Fernández-Vizarra Erika ◽  
Ding Shujing ◽  
...  
Keyword(s):  
Ribosomal Proteins ◽  
Nadh Dehydrogenase ◽  
Inner Mitochondrial Membrane ◽  
True Nature ◽  
Respiratory Chain Deficiency ◽  
Total Absence ◽  
Metabolic Labelling ◽  
Ideal System ◽  
Oxphos System ◽  
Early Phases

ABSTRACTOxidative phosphorylation (OXPHOS) system localized in the inner mitochondrial membrane secures production of the majority of ATP in mammalian organisms. Individual OXPHOS complexes were shown to form supramolecular assemblies termed supercomplexes. It has been repeatedly shown that complexes are not linked only by their function but also by interdependence of individual complex biogenesis or maintenance. For instance, cytochrome c oxidase (cIV, COX) or cytochrome bc1 complex (cIII) deficiencies affect the level of fully assembled NADH dehydrogenase (cI) in monomer as well as within supercomplexes. It was hypothesized that cI is affected at the level of enzyme assembly as well as at the level of cI stability and maintenance. However, the true nature of interdependency between cI and cIV is not fully understood yet. We used HEK293 cellular model with complete knockout of COX4 subunit, which serves as an ideal system to study interdependency of cI and cIV, as early phases of cIV assembly process are disrupted. Total absence of cIV was accompanied by profound deficiency of cI, documented by selective decrease in cI subunits amount and significantly reduced amount of assembled cI. Supercomplexes assembled from cI, cIII and cIV were missing in COX4dKO due to loss of cIV and decrease in cI amount. Pulse-chase metabolic labelling of mtDNA-encoded proteins uncovered decrease of cIV and cI subunits translation. Moreover, partial impairment of mitochondrial proteosynthesis correlated with decreased level of mitochondrial ribosomal proteins. In addition, complexome profiling approach uncovered accumulation of cI assembly intermediates indicating that cI biogenesis was affected rather than stability. We propose that impairment of mitochondrial proteosynthesis caused by cIV deficiency represents one of the mechanisms which may couple biogenesis of cI and cIV.

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