Eukaryotes / Mitochondria / Sexual Reproduction / Death

Eukaryogenesis: a symbiosis between an archeon and a bacterium. The endosymbiotic bacteria became the eukaryotic cell's mitochondria, providing most of the energy of the cell.
Sexual reproduction: it is believed that true sexual production arose in the last eukaryotic common ancestor. There seems to be a strong correlation between the presence of mitochondria and sexual reproduction.

Now a new study The role of mitochondria in sex- and age-specific gene expression in a species without sex chromosomes doi:10.1073/pnas.2321267121 (biorxiv 2023.12.08.570893v1):

Our results suggested sex-specific tradeoffs between energy production and mitochondrial maintenance, and association of mitochondrial expression with lifespan. In this species where sex bias cannot be confounded with the effects of sex chromosomes, males and females were found to experience widely different mitochondrial and mito-nuclear effects on gene expression and aging.

Gentle but reasonably precise exposition by Darrin S. Joy, University of Southern California.

Apoptosis#

(From Highlight: Unlocking the Ancient Origins of Cell Death)

Apoptosis, often referred to as programed cell death, is a fundamental process crucial to the growth and development of multicellular organisms. This process, or a primordial form of it, is also observed in single-celled eukaryotes like yeast and other microeukaryotes (aka protists).

In a new study published in Genome Biology and Evolution, scientists from the Institute of Biochemistry and Biophysics of the Polish Academy of Sciences reveal that many apoptotic factors may trace their origins to the time of mitochondrial domestication, suggesting remarkable conservation over the span of 1.8 billion years (Kaushal et al. 2023).

The study’s findings further support an endosymbiotic origin of apoptosis, a hypothesis that was first proposed by Guido Kroemer in 1997 (Kroemer 1997). Kroemer suggested that the bacterial precursors of mitochondria produced both toxins (apoptotic factors) and antitoxins (anti-apoptotic factors). In this scenario, the antitoxins acted as “addiction molecules,” ensuring the persistence of the symbiont. Driven by this evolutionary conflict between bacterial endosymbionts and hosts, the toxins eventually evolved into the apoptotic factors we recog- nize today.
Kaczanowski and Zielenkiewicz present an alternative scenario for the evolution of apoptosis. They propose that early protoeukaryotes were predators, relying on bacterial prey. These bacteria, in response to predation, produced toxins as a defense mechanism. Over time, these bacteria were domesticated to serve as mitochondria within eukaryotic cells, and their toxins evolved into apoptotic factors. The different families of AIFs present today and their sporadic distribution across distantly related eukary otes suggest the existence of multiple redundant toxins in the protomitochondria and hint at a coevolutionary arms race between protomitochondria and their protoeukaryotic hosts.

Deactivation of X chromosome#

X-chromosome inactivation was discovered in 1961 by the British geneticist Mary Lyon, and is sometimes called Lyonization,

While the other twenty-two chromosomes are essentially duplicated in both males and females, then, females have two X chromosomes to males' one. To cope with that disparity, every cell in the female body deactivates the entirety of one of its two X chromosomes.

The deactivation is random: either paternal or maternal. At approximately the time of embryonic implantation, one of the two X chromosomes in each cell of the female embryo is randomly selected for inactivation.

Once an X chromosome is inactivated it will remain inactive throughout the lifetime of the cell and its descendants in the organism (its cell line); Cells undergo transcriptional and epigenetic changes to ensure this inactivation is permanent
Commonly, X-inactivation is unevenly distributed across the cell lines within one organism