  This paper summarizes previous work linking protein aggregation to the
heterozygosity of organisms. It also cites the literature showing a correlation
between species' morphological complexity and the lengths of their proteins.
These two findings are combined to form a theory that may potentially explain
the ploidy levels of organisms. Organisms can employ heterozygosity to inhibit
protein aggregation. Hence, complex organisms tend to be diploid because they
tend to synthesize long, aggregation-prone proteins. On the other hand, simple
organisms tend to be haploid because they synthesize short proteins that are
less prone to aggregation. The theory may also explain ecological trends
associated with organisms of different ploidy level. Two mathematical models
are also developed that may explain: 1) how protein aggregation results in
truncation selection that maintains numerous polymorphisms in natural
populations, and 2) the relationship between protein turnover, metabolic
efficiency, and heterosis.
