Biology Reference
In-Depth Information
reducing the risk for haploinsufficiency. At a few loci, however, parent-of-origin informa-
tion persists through development, via maintenance and protective complexes. In this
review, we discuss the parental asymmetries that are inherited from the gametes, the
forces involved in their elimination, reinforcement or protection, and how this influ-
ences the embryonic program. We highlight the gradual loss of all parental asymmetries
occurring throughout development, except at imprinted loci, which maintain distinct
parent-of-origin chromatin and transcriptional characteristics for life. A deeper under-
standing of the nongenetic contributions of each germline is important to provide
insight into the origin of non-Mendelian inheritance of phenotypic traits, as well as
the risk of incompatibilities between parental genomes.
1. INTRODUCTION
The reproductive cells, the oocyte and the spermatozoon, are specialized
to transmit genetic material across generations through the process of fertiliza-
tion. While this function is equally shared between the two parental gametes,
essential pools of proteins and mitochondria are uniquely inherited from the
oocyte. The maternal ooplasm is notably required for supporting early devel-
opment before the activation of the embryonic genome. Because the oocyte
and the sperm harbor vastly different types of chromatin and carry different
sets of RNA populations (
Bourc'his & Voinnet, 2010; Gill, Erkek, & Peters,
2012
), the potential for additional parental asymmetry in the early embryo is
tremendous. In this chapter, we focus on nongenetically encoded information
contained in the nucleus in the formof biochemical modifications imposed on
the DNA molecule itself and on its supporting proteins, the histones. Because
this information is intrinsically tied to the genetic material, it is more likely to
persist longer after fertilization and to be maintained in an epigenetic manner
throughout cell divisions in the newly developing individual and potentially to
adulthood. Unraveling the origin, targets, and consequences of parent-specific
information is key to understanding complex phenotypic traits inmammals, in
particular, forms of non-Mendelian inheritance. Important insights can also be
gained from deciphering the duration of parental epigenetic asymmetries and
the forces exerted to reduce or protect their occurrence throughout life.
1.1. Flexibility of histone-associated information
Histone-borne information encompasses a very complex system of various
redundant, exclusive, and complementary post-translational modifications
mainly localized to the N-terminal tails, which freely extrude from the nucle-
osomes. These modifications can alter gene expression via direct effects on
