Biology Reference
In-Depth Information
C. reinhardtii
genome, four of these putative genes have been annotated as
truncated globin-like proteins and given the designation 'THB'; THB1
(ORF 81856), THB2 (ORF 196750), THB3 (ORF 145701) and THB4
(ORF 145700), which have been given Uniprot identifiers A8JAR4,
A8JAR3, A8ISQ0 and A8ISP8, respectively. Within the nuclear genome,
genes
THB1
and
THB2
are located together on chromosome 14 while
THB3
and
THB4
are located together on chromosome 4. Both THB1
and THB2 show high similarity to CtrHb (81% and 79%, respectively);
in contrast, THB3 and THB4 similarities are lower (64% and 73%, respec-
tively). One of the putative proteins from these genes (THB4) has a potential
transit peptide that suggests chloroplast targeting (
Tardif et al., 2012
), while
THB1 does not appear to have any potential transit peptide (E. Johnson,
personal observation).
In addition to having a low similarity to known TrHbs, THB3 is missing
some conserved residues found in TrHb1 proteins, notably the proximal his-
tidine (
Fig. 6.5
). This histidine is thought to be essential for haem binding;
however, a handful of globin sequences (approximately 1-5%) do not possess
this residue even though the remainder of the sequence aligns very well with
known globin proteins (
Vinogradov et al., 2013
). Whether these proteins are
capable of haem binding, whether they associate with a different cofactor, or
what function they might have, if any, remains to be determined.
The four THB genes mentioned above are for predicted proteins, but the
product of one of these genes, THB1, has been tentatively located within the
cell. In a study by
Lechtreck et al. (2009)
, THB1 was found to accumulate in
the flagella of
C. reinhardtii
strains impaired in intraflagellar transport (IFT).
These strains are defective in a protein complex termed the BBSome, which
is linked to a rare human disorder known as Bardet-Biedl syndrome
(
Tobin & Beales, 2007; Zaghloul & Katsanis, 2009
). This syndrome has
itself been linked to cilia defects, and BBSomes are believed to be involved
in IFT trafficking (
Beales, 2005; Rosenbaum & Witman, 2002
).
Specifically, the strain used in the Lechtreck study is defective in the
BBS4
gene and exhibits a non-phototactic phenotype, meaning that the
Chlamydomonas
cells cannot perform the native alteration of its directional
motility following changes in light direction or intensity. The genetic trans-
formation of the
bbs4
strain with a native
BBS4
gene restored the strong
phototaxis characteristics of the parental strain. Further screening reveals
the same phenotype from additional strains, as deletions within genes
BBS1
and
BBS7
(also linked to BBSome complex) resulted in loss of pho-
totaxis. Analysis of these strains showed that the loss of BBSome function
