Biology Reference
In-Depth Information
capitata
, and
Drosophila
(
Bownes 1986, Rina and Savakis 1991, Trewitt et al.
1992
). The fat body of the mother is the primary producer of yolk proteins, but
some yolk proteins are synthesized by the follicular epithelium of the ovary in
D. melanogaster
.
Yolk proteins in
Drosophila
consist of three polypeptides: YP1, YP2, and YP3.
YP1 is expressed by the fat body and, after posttranslational processing and gly-
cosylation, the proteins are secreted into the hemolymph and delivered to the
oocyte. YP2 is expressed in ovaries. The production and delivery of the three
proteins are coordinately regulated and under the control of two hormones,
20-hydroxyecdysone and juvenile hormone (
Bownes 1986
). These two hormones
also regulate molting and metamorphosis during development.
Production of yolk proteins begins during the first day of
Drosophila
adult
life. The production rate is high, with yolk proteins representing
≈
1
⁄
3
of the total
proteins in the hemolymph. YP1 and YP2 are closely linked genes on the X chro-
mosome, whereas YP3 also is sex-linked but more distant. YP1 and YP2 show
much sequence homology and probably resulted from a fairly recent gene dupli-
cation event. Only one small intron is found in YP1 and YP2, and two introns in
YP3. Extensive yolk-protein synthesis in
Drosophila
is achieved because tissues
are polytene and polyploid.
4.9.8 Transposable Elements
Transposable elements (TEs) are middle-repetitive DNA sequences that can move
(transpose) to new sites, invert, and undergo deletion or amplification (
Berg and
Howe 1989, Finnegan 1989
). TEs may cause damage in genomes and must estab-
lish in the germ line to be maintained in the population, so they are considered
“selfish elements.” Organisms have several mechanisms of reducing the impact
of TEs on their genomes (
Blumenstiel 2011
,
Levin and Moran 2011
). For exam-
ple, host DNA that is methylated inhibits transcription of TEs. Small RNAs (small
interfering RNAs [siRNAs] and Piwi-interacting RNAs [piRNAs]) defend against
TEs (
Blumenstiel 2011
). As one might expect, TEs counter these defense mecha-
nisms in their hosts when mobilizing in germ cells or during early development.
The evolution of suppression systems in the host can result in an evolutionary
arms race that drives a high rate of evolution in the TEs.
TEs are not always bad for a genome. They can generate genetic variability,
sometimes they can acquire useful functions in genomes, and they can mod-
ify genome structure and functions, resulting in diversity upon which evolu-
tion can act (
Feschotte and Pritham 2007, Blumenstiel 2011, Werren 2011
). In
fact, Biemont (2009) proposes that TEs are important in chromatin formation
