bims-plasge 2024-08-18 papers

Issue of 2024–08–18
two papers selected by
Vera S. Bogdanova, ИЦиГ СО РАН

Int J Mol Sci. 2024 Jul 31. pii: 8372. [Epub ahead of print]25(15):

A Systematic Review and Developmental Perspective on Origin of CMS Genes in Crops.

Xuemei Zhang, Zhengpin Ding, Hongbo Lou, Rui Han, Cunqiang Ma, Shengchao Yang.

Cytoplasmic male sterility (CMS) arises from the incompatibility between the nucleus and cytoplasm as typical representatives of the chimeric structures in the mitochondrial genome (mitogenome), which has been extensively applied for hybrid seed production in various crops. The frequent occurrence of chimeric mitochondrial genes leading to CMS is consistent with the mitochondrial DNA (mtDNA) evolution. The sequence conservation resulting from faithfully maternal inheritance and the chimeric structure caused by frequent sequence recombination have been defined as two major features of the mitogenome. However, when and how these chimeric mitochondrial genes appear in the context of the highly conserved reproduction of mitochondria is an enigma. This review, therefore, presents the critical view of the research on CMS in plants to elucidate the mechanisms of this phenomenon. Generally, distant hybridization is the main mechanism to generate an original CMS source in natural populations and in breeding. Mitochondria and mitogenomes show pleomorphic and dynamic changes at key stages of the life cycle. The promitochondria in dry seeds develop into fully functioning mitochondria during seed imbibition, followed by massive mitochondria or mitogenome fusion and fission in the germination stage along with changes in the mtDNA structure and quantity. The mitogenome stability is controlled by nuclear loci, such as the nuclear gene Msh1. Its suppression leads to the rearrangement of mtDNA and the production of heritable CMS genes. An abundant recombination of mtDNA is also often found in distant hybrids and somatic/cybrid hybrids. Since mtDNA recombination is ubiquitous in distant hybridization, we put forward a hypothesis that the original CMS genes originated from mtDNA recombination during the germination of the hybrid seeds produced from distant hybridizations to solve the nucleo-cytoplasmic incompatibility resulting from the allogenic nuclear genome during seed germination.

Keywords: chimeric mitochondrial gene; distant hybridization; mitochondrial fusion and fission; mtDNA recombination; original CMS source; seed germination

DOI: https://doi.org/10.3390/ijms25158372

Mol Biol Rep. 2024 Aug 16. 51(1): 910

Insights into cellular crosstalk regulating cytoplasmic male sterility and fertility restoration.

Harnoor Kaur Dhillon, Madhu Sharma, A S Dhatt, O P Meena, Jiffinvir Khosa, M K Sidhu.

Cytoplasmic male sterility has been a popular genetic tool in development of hybrids. The molecular mechanism behind maternal sterility varies from crop to crop. An understanding of underlying mechanism can help in development of new functional CMS gene in crops which lack effective and stable CMS systems. In crops where seed or fruit is the commercial product, fertility must be recovered in F1 hybrids so that higher yield gains can be realized. This necessitates the presence of fertility restorer gene (Rf) in nucleus of male parent to overcome the effect of sterile cytoplasm. Fertility restoring genes have been identified in crops like wheat, maize, sunflower, rice, pepper, sugar beet, pigeon pea etc. But in crops like eggplant, bell pepper, barley etc. unstable fertility restorers hamper the use of Cytoplasmic genic male sterility (CGMS) system. Stability of CGMS system is influenced by environment, genetic background or interaction of these factors. This review thus aims to understand the genetic mechanisms controlling mitochondrial-nuclear interactions required to design strong and stable restorers without any pleiotropic effects in F1 hybrids.

Keywords: Aldehyde dehydrogenase; Cytoplasmic male sterility; Fertility restorer; Glycine rich proteins; Pentatricopeptide repeats (PPR); Restorer of fertility like (RFL) proteins

DOI: https://doi.org/10.1007/s11033-024-09855-1