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ANCIENT GENE RECRUITMENT. "One prediction that can be made from the antithetic theory is that the evolution of the sporophyte involved the recruitment of ancient genes and regulatory networks from the pre-existing gametophyte generation; these networks would then diversify and promote morphological diversification in the sporophyte generation." Supported by transcriptomic studies. http://rstb.royalsocietypublishing.org/content/367/1588/508.short View in LinkedIn

ANTITHETICAL THEORY. "The sporophyte originated through the intercalation of mitotic divisions in the zygote before meiosis, resulting in a diploid embryo being retained on a gametophytic thallus; the sporophyte would then gradually evolve from a parasitic dependence on the gametophyte into a dominant, physiologically independent organism. The antithetic theory is supported by the dominance of gametophytes over sporophytes in bryophytes and by the absence of sporophytes in charophyte algae." http://rstb.royalsocietypublishing.org/content/367/1588/508.short View in LinkedIn

SEVERAL APPEARANCES. "Land plants (embryophytes) evolved from freshwater multicellular algae, probably related to the extant charophyte groups Charales or Coleochaetales. An alternation of two multicellular generations has evolved several times in different groups of algae but it appears to have evolved only once in the streptophytes." https://lnkd.in/dNCxaKS View in LinkedIn

FIRST APPEARANCE. "A life history involving alternation of two developmentally associated, multicellular generations (sporophyte and gametophyte) is an autapomorphy of embryophytes (bryophytes + vascular plants). Microfossil data indicate that Mid–Late Ordovician land plants possessed such a life cycle, and that the origin of alternation of generations preceded this date." (450-475 My ago). https://lnkd.in/dF6EXUX View in LinkedIn

HAPLOID-DIPLOID LIFE CYCLE. "Unlike animals, land plants undergo an alternation of generations, producing multicellular bodies in both haploid (1n: gametophyte) and diploid (2n: sporophyte) generations. Plant body plans in each generation are regulated by distinct developmental programs initiated at either meiosis or fertilization, respectively." http://www.sciencedirect.com/science/article/pii/S1534580713000427 View in LinkedIn

JUMPING GENES. “However, in response to a potential decay of the chromatin structure during aging, excess retrotransposon transcription prevents recruitment of cohesion and condensin, causing persistent DNA damage checkpoint activation and senescence.” http://journal.frontiersin.org/article/10.3389/fgene.2013.00136/full View in LinkedIn

SO ENDS this first of two weekends on plant alternation of generations. That such a complex system exists is in part due to the necessity of not increasing chromosome numbers during successive generations, as well as the cobbling together of available tools that were handy. Evolution is a zig zaggy chaotic process with many dead ends and mistakes. Nothing was purpose-built. View in LinkedIn

BACK TO CHROMATIN. “Telomere-mediated activation of the DNA damage response appears to be intimately linked to the chromatin structure. Specifically, it was shown that chronic DNA damage from the processed telomeres also affects histone expression leading to their depletion and to the depletion of the central histone chaperones.” http://journal.frontiersin.org/article/10.3389/fgene.2013.00136/full View in LinkedIn

DIFFERENT HELPER CELL GROUPS. "Depending on their sex and their stage of development, plant reproductive cell lineages are associated with different supporting cell populations. In the stamen, male meiotic cells are invested by a layer of sporophytic (somatic) tapetal cells, which are essential for postmeiotic development and, particularly, the synthesis of the sporopollenin pollen wall and its coating." http://www.sciencedirect.com/science/article/pii/S1534580713000427 View in LinkedIn

TELOMERES AND DNA DAMAGE. “Telomere length is highly connected with the replicative lifespan of metazoan cells. Telomeres shorten with each successive round of DNA replication until one telomere reaches a threshold of “shortness” that emits a chronic DNA damage signal that causes the cell to cease dividing and enter senescence. Mechanistically, the short telomeres are seen as chronic DNA damage by the cell, resulting in the activation of the DNA damage response, which causes a G1 cell cycle arrest.” http://journal.frontiersin.org/article/10.3389/fgene.2013.00136/full View in LinkedIn