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about 30,000 genes ( Srivastava et al., 2010 ), while a cnidarian, Hydra littoralis , is
believed to have only about 13,000 genes. Sponges have more genes than humans
do and share about 70% of their genes with humans ( Stout et al., 2007 ). They also
have genes for the cell types and tissues they lack, such as muscle cells and neurons.
Mocking conventional biological thought the evolution of sponges and eumetazoans
from the Urmetazoa “required” a loss in the number of genes ( Harcet et al., 2010 ).
Sponges use developmentally important cell signaling and adhesion genes are
involved in the morphogenetic processes in higher invertebrates and even verte-
brates, from worms to humans ( Nichols et al., 2006 ). For example, Oscarela car-
mela expresses many of the signaling genes and has all but one (the nuclear hormone
receptor pathway) of the seven major bilaterian signaling pathways: Wnt, TGF-β,
Hedgehog, receptor tyrosine kinase, Jak/STAT, nuclear hormone receptor, and Notch,
which are responsible for the development of limbs, eyes, vertebrate segmentation, and
for the assembly of neural circuits in bilaterians ( Nichols et al., 2006 ). Sponges also
have hormones that may be involved in their growth and reproduction.
Such data speak unambiguously against any correlation or causal relationship
between genome's size or gene number and the structural complexity or evolutionary
progress in Animalia . What are sponges missing that would have changed their fate
as a dead end of evolution?
That eumetazoans, such as cnidarians, also evolved other types of cells such as
muscle cells, epithelial, dermal, and other cells is a water cooler topic to the main
problem of the evolution of a centralized ICS that is necessary to develop and main-
tain the complex biological structures of eumetazoans. The absence of a centralized
control system in sponges can explain why they lack precise morphology, symme-
try, or size as eumetazoans do. Their morphology and size are determined in part by
physical factors (viscoelasticity, differential cell adhesivity, biochemical diffusion,
etc.) ( Newman and Müller, 2000 ) and in part by their “obscure” control system at the
supracellular level ( Cabej, 2008, 2012 ), a type of “paracrine prenervous system” that
is responsible for their contractility in response to various stimuli ( Nickel, 2010 ).
It is very likely that the most salient difference between them and eumetazoans is
that the last succeeded in evolving a different cell type, the neuron, and the resulting
nervous system ( Cabej, 1999, 2004; Stanley, 1992 ). 3
3 Recently, I found that Steven M. Stanley was the irst to propose the possible role of the neuron as
an intrinsic driver of the animal evolution, in a short but insightful 1992 article in the little accessible
Geological Society of America Abstracts with Programs . Deviating from the mainstream biological
thought that looked into extrinsic environmental factors as the cause of the delay of adaptive radiation,
Stanley suggested that the “boring” delay of evolutionary progress and innovations for hundreds of mil-
lions of years was caused by an intrinsic barrier:
A likely barrier was the difficulty of evolving the neuron. Prior to the origin of the neuron, effective use
of muscles for feeding and locomotion was impossible; preneural animals could not have evolved in
grade far beyond the extant Placozoa. The neuron is highly complex, employing a positive feedback sys-
tem, and is quite similar among all animal taxa, from jellyfishes to humans. Thus, the neuron was almost
certainly of monophyletic origin and should be viewed as a defining trait for the Metazoa . Sponges
illustrate the limitations of evolution sans (without - N.C.) neurons, having existed in a state of adaptive
stagnation for more than half a billion years as simple, sessile creatures that feed via single cells.
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