“…The second model (White, 1973) proposed that B chromosomes may be maintained in the population without drive mechanisms if they have a beneficial effect on their carriers in small numbers but start to be detrimental in high copy numbers. Empirical data reviewed in this paper supports both models providing evidence for the selfish spread of B chromosomes in populations through drive in many species ( Hasegawa, 1934 ; Nur, 1962 ; Nur, 1963 ; Rutishauser and Rӧthlisberger, 1966 ; Nur, 1969 ; Kayano, 1971 ; Jones and Rees, 1982 ; Gregg at al., 1984 ; Murray, 1984 ; Viseras et al, 1990 ; Jones, 1991 ; Pardo et al, 1995 ; Houben, 2017 ; Jones, 2018 ; Clark and Kocher, 2019 ; Blavet et al, 2021 ) as well as identifying beneficial effects of B chromosomes for their hosts ( Williams, 1970 ; Dherawattana and Sadanaga, 1973 ; Rees and Hutchinson, 1974 ; Holmes and Bougourd, 1989 ; Miao et al, 1991 ; Plowman and Bougourd, 1994 ; Enkerli et al, 1997 ; Hatta et al, 2002 ; Nokkala et al, 2003 ; Rodriguez-Carres et al, 2008 ; Akagi et al, 2009 ; Coleman et al, 2009 ; Ma et al, 2010 ; Balesdent et al, 2013 ; Thatcher et al, 2016 ; Williams et al, 2016 ; Dalíková et al, 2017 ; Pereira et al, 2017 ; van Dam et al, 2017 ; Armitage et al, 2018 ; Kinsella et al, 2019 ; Torgasheva et al, 2019 ; Imarazene et al, 2021 ; Lewis et al, 2021 ). From the example in rye where B chromosomes have beneficial function but are still driving ( Pereira et al, 2017 ) we see that there could be even co-occurrence of drive and beneficial function which indicates the rather extensive complexity of B chromosome evolution.…”