Chromatin assembly factor 1 subunit
p55 is observed mainly in the nuclei of syncytial blastoderm embryos (nuclear cycle 13) in both S or M phases. After cellularization, p55 appears to be nuclear except during M phase, in which it is present throughout the cell, possibly as a consequence of the partial breakdown of the nuclear envelope during mitosis. The level of p55 is highest during early embryogenesis and then decreases by a factor of approximately 10 in larvae, pupae, and adults. The amount of protein present in early embryos corresponds to about 220,000 molecules per nucleus, based on an estimated average of 12,000 nuclei per embryo. Thus p55 is a relatively abundant protein (Tyler, 1996).
Many proteins have been proposed to be involved in retinoblastoma protein (pRB)-mediated repression, but it is largely uncertain which cofactors are essential for pRB to repress endogenous E2F-regulated promoters. Advantage was taken of the stream-lined Drosophila dE2F/RBF pathway, which has only two E2Fs (dE2F1 and dE2F2), and two pRB family members (RBF1 and RBF2). With RNA interference (RNAi), potential corepressors were depleted and the elevated expression of groups of E2F target genes that are known to be directly regulated by RBF1 and RBF2 was sought. Previous studies have implicated histone deacetylase (HDAC) and SWI/SNF chromatin-modifying complexes in pRB-mediated repression. However, the results fail to support the idea that the SWI/SNF proteins are required for RBF-mediated repression and suggest that a requirement for HDAC activities is likely to be limited to a subset of targets. The chromatin assembly factor p55/dCAF-1 is essential for the repression of dE2F2-regulated targets. The removal of p55 deregulates the expression of E2F targets that are normally repressed by dE2F2/RBF1 and dE2F2/RBF2 complexes in a cell cycle-independent manner but has no effect on the expression of E2F targets that are normally coupled with cell proliferation. The results indicate that the mechanisms of RBF regulation at these two types of E2F targets are different and suggest that p55, and perhaps p55's mammalian orthologs RbAp46 and RbAp48, have a conserved function in repression by pRB-related proteins (Taylor-Harding, 2004).
Dendrite arborization patterns are critical determinants of neuronal function. To explore the basis of transcriptional regulation in dendrite pattern formation, RNA interference (RNAi) was used to screen 730 transcriptional regulators and 78 genes involved in patterning the stereotyped dendritic arbors of class I da neurons were identified in Drosophila. Most of these transcriptional regulators affect dendrite morphology without altering the number of class I dendrite arborization (da) neurons and fall primarily into three groups. Group A genes control both primary dendrite extension and lateral branching, hence the overall dendritic field. Nineteen genes within group A act to increase arborization, whereas 20 other genes restrict dendritic coverage. Group B genes appear to balance dendritic outgrowth and branching. Nineteen group B genes function to promote branching rather than outgrowth, and two others have the opposite effects. Finally, 10 group C genes are critical for the routing of the dendritic arbors of individual class I da neurons. Thus, multiple genetic programs operate to calibrate dendritic coverage, to coordinate the elaboration of primary versus secondary branches, and to lay out these dendritic branches in the proper orientation (Parrish, 2006; Full text of article).
To assay for the stereotyped dendrite arborization pattern of class I da neurons (hereafter referred to as class I neurons) in RNAi-based analysis of dendrite development, a Gal4 enhancer trap line (Gal4221) was used that is highly expressed in class I neurons and weakly expressed in class IV neurons during embryogenesis. Because of the simple and stereotyped dendritic arborization patterns of the dorsally located ddaD and ddaE, the studies of dendrite development focused on these two dorsally located class I neurons (Parrish, 2006).
To establish that RNAi is an efficient method to systematically study dendrite development in the Drosophila embryonic PNS, it was demonstrated that injecting embryos with double-stranded RNA (dsRNA) for green fluorescent protein (gfp) is sufficient to attenuate Gal-4221-driven expression of an mCD8::GFP fusion protein as measured by confocal microscopy. Next whether RNAi could efficiently phenocopy loss-of-function mutants known to affect dendrite development was tested. Similar to the mutant phenotype of short stop (shot), which encodes an actin/microtubule cross-linking protein, shot(RNAi) caused routing defects, dorsal overextension, and a reduction in lateral branching of dorsally extended primary dendrites. Likewise, RNAi of sequoia or flamingo resulted in overextension of ddaD and ddaE, RNAi of hamlet resulted in supernumerary class I neurons, and RNAi of tumbleweed resulted in supernumerary class I neurons and a range of arborization defects, consistent with the reported mutant phenotypes. Thus, RNAi is effective in generating reduction of function phenotypes in embryonic class I dendrites (Parrish, 2006).
RNAi of the Polycomb group (PcG) genes Su(z)12, E(z), esc, or Caf1 similarly caused an increase in branch number and an expansion of the receptive field of class I neurons. Consistent with the similar RNAi phenotypes for these genes, Su(z)12, E(z), esc, and Caf1 are components of the multiprotein esc/E(z) polycomb repressor complex. One critical role for PcG-mediated gene silencing is the regulation of hox gene expression. Therefore, Polycomb-mediated regulation of hox gene expression likely contributes to arborization of class I neurons (Parrish, 2006).
In vitro data suggest that the human RbAp46 and RbAp48 genes encode proteins involved in multiple chromatin remodeling complexes and are likely to play important roles in development and tumor suppression. However, to date, understanding of the role of RbAp46/RbAp48 and its homologs in metazoan development and disease has been hampered by a lack of insect and mammalian mutant models, as well as redundancy due to multiple orthologs in most organisms studied. This study reports the first mutations in the single Drosophila RbAp46/RbAp48 homolog Caf1, identified as strong suppressors of a senseless overexpression phenotype. Reduced levels of Caf1 expression result in flies with phenotypes reminiscent of Hox gene misregulation. Additionally, analysis of Caf1 mutant tissue suggests that Caf1 plays important roles in cell survival and segment identity, and loss of Caf1 is associated with a reduction in the Polycomb Repressive Complex 2 (PRC2)-specific histone methylation mark H3K27me3. Taken together, these results suggest suppression of senseless overexpression by mutations in Caf1 is mediated by participation of Caf1 in PRC2-mediated silencing. More importantly, the mutant phenotypes confirm that Caf1-mediated silencing is vital to Drosophila development. These studies underscore the importance of Caf1 and its mammalian homologs in development and disease (Anderson, 2011).
Several lines of evidence suggest that the participation of Caf1 in PcG complexes may account for many of the phenotypes observed in flies with altered expression of Caf1. First, Caf1 loss-of-function clones in the eye have phenotypes ranging from slight disorganization and bristle defects to almost complete loss of homozygous tissue in adults, and incomplete rescue of Caf1 results in adult eyes that are small and disorganized. Clones of many PcG genes have similar phenotypes in the eye. Loss of E(z) or Pc causes mild defects in differentiation in the third instar disc, but clones fail to survive in adults. An analogous situation occurs in Caf1short clones, where expression of Elav, which marks differentiating neurons, is present in Caf1 clones at third instar but Caf1short tissue is largely missing in the adult. Derepression of Hox genes could account for these phenotypes, as ectopic expression of many Hox genes in the eye field causes small disorganized eyes in adults (Anderson, 2011).
Second, flies with incomplete rescue of Caf1 display a range of homeotic phenotypes, notably transformation of arista to leg. Similar homeotic transformations, including antenna-to-leg transformations, are a hallmark of mutations in PcG genes. Also a genetic interaction was observe between Caf1 and the PRC1 gene Pc, since mutations in Caf1 are able to dominantly suppress the homeotic transformation of second or third leg to first leg in Pc15/+ males (Anderson, 2011).
Third, the disrupted patterning of Caf1short mutant heads may also result from PcG dysfunction. It is possible that these patterning defects are non-cell autonomous and may be an indirect result of widespread apoptosis in the eye disc. Normally, when an imaginal disc is injured, remaining cells proliferate and assume correct identities, leading to a perfectly patterned adult structure. This type of regeneration requires that some determined cells must change their fates and involves substantial chromatin remodeling. Under specific circumstances, the disc can regenerate with incorrect patterning, leading to duplication, deletion or transformation of structures, a phenomenon referred to as transdetermination. Levels of many PcG transcripts are increased in transdetermining imaginal discs, and heterozygous mutations in PcG genes can enhance transdetermination in regenerating imaginal discs. Therefore, one interpretation of the patterning defects in Caf1short mutant discs is that under the stress of widespread apoptosis, the remaining heterozygous tissue is haploinsufficient for the chromatin remodeling activity required to properly regenerate and pattern the injured disc. Consistent with this interpretation, no extra or missing appendages are observed in flies with Caf1long clones, which show less active Caspase 3 staining at third instar (Anderson, 2011).
Finally, in Caf1 mutant tissue, a reduction is observed in levels of the H3K27me3 mark, which is associated with inactive chromatin and PRC2 activity. These data are consistent with a disruption of PRC2 function as a result of loss of Caf1 and represent the first in vivo evidence that Caf1 is an essential member of this chromatin remodeling complex in an animal model (Anderson, 2011).
One obvious question arises from the current study: why were multiple Caf1 alleles identified in a screen for modifiers of the sens overexpression phenotype? Moreover, it is surprising that mutations in Caf1 were not identified in previous Drosophila modifier screens involving PcG or Rb pathway members. It is proposed that the link between sens and Caf1 is due to the role of Caf1 in PcG-mediated silencing (Anderson, 2011).
Recent evidence suggests that Sens and Hox proteins can compete for binding at overlapping sites at an enhancer of the rhomboid (rho) locus (Li-Kroeger, 2008). When the Hox protein Abdominal-A (Abd-A) binds, transcription of rho is activated, whereas binding by Sens leads to repression of rho. In the embryo, this mechanism acts as a molecular switch to allow differentiation of either chordotonal organs (under control of Sens) or hepatocyte-like cells called oenocytes (by the action of Abd-A). It is proposed that a similar mechanism underlies the suppression of the Sens overexpression phenotype. It is hypothesized that one or more targets of Sens in the eye contain similar overlapping sites that can be bound by either Sens or a Hox protein. During normal development, these loci are bound by neither Sens nor Hox in undifferentiated cells posterior to the furrow, as no Hox genes are known to be widely expressed in the eye field. In the absence of both types of factors, these loci are transcriptionally active, and are necessary to ultimately attain the proper fates of the cells in which they are expressed. When Sens is overexpressed, as in ls, Sens binds to its recognition site in the downstream loci, repressing transcription. Repression of these genes initiates a cascade leading to a change in cell fate; for example, some of the cells that would normally become secondary or tertiary pigment cells now become bristle precursors, giving rise to the extra bristles of ls. However, when one copy of Caf1 is lost, a slight derepression of the Hox genes occurs due to loss of PcG activity. Hox proteins are now able to compete with Sens for the overlapping binding sites, tipping the balance towards activation of downstream genes and attainment of normal cell fate - effectively suppressing ls. The ability of ectopic expression of pb and Antp in the eye to suppress ls is consistent with this hypothesis. Suppression of ls by Hox proteins is particularly significant given that ectopic expression of Antp alone in the eye field leads to a small and disorganized eye. As Sens activity is exquisitely sensitive to Hox proteins, especially in the eye, the screen for modifiers of a sens overexpression phenotype was therefore ideal for identifying mutations in Caf1 (Anderson, 2011).
Previous studies have explored pro-apoptotic roles of Hox proteins and anti-apoptotic roles of Sens. It is therefore possible that one effect of Hox gene derepression in ls eyes suppressed by Caf1 may be restoration of an apoptotic fate in cells that would otherwise form bristle precursors due to ectopic Sens. Abd-A expression in the abdomen during normal third instar larval development leads to apoptosis of proliferating neuroblasts of the central nervous system, and ectopic expression of other Hox genes can also cause neuroblast apoptosis. Accordingly, survival of neuroblasts is dependent on PcG activity to repress Hox gene expression. Furthermore, expression of Sens is necessary in the Drosophila embryonic salivary gland to prevent apoptosis. Thus, one possible mechanism for suppression of ls by Caf1 mutations is that in the ls eye, Sens may promote the ectopic bristle fate partly by repressing apoptotic genes in cells normally fated to die, whereas in the ls eye suppressed by mutations in Caf1, ectopic Hox proteins may promote apoptosis and prevent bristle formation. Increased Ubx expression was not detected by antibody staining; however, a very small increase in one or more Hox proteins may be all that is necessary to change the transcriptional state of downstream loci and prevent the ectopic bristles and other defects in the highly sensitized ls eye - especially in the eye field, where no Hox genes are known to be highly expressed. Furthermore, the fact that multiple Hox proteins can recognize the same DNA binding site offers the possibility that the competitive effect of each Hox protein type on genes with overlapping Sens/Hox binding sites would be additive. Therefore, although loss of one copy of Caf1 may only cause a small derepression of any one Hox gene, mild derepression of many Hox genes collectively can lead to strong repression of the ls phenotype (Anderson, 2011).
Biochemical evidence suggests that Caf1 is a member of multiple complexes that effect gene regulation through chromatin remodeling, suggesting that it is a vital component of the cell's arsenal of chromatin modifying factors. Although the results suggest that disruption of PRC2 function may be the most important consequence of Caf1 gain- or loss-of-function, many phenotypes that were observed in Caf1 mutant tissue are also reminiscent of mutations in members of other complexes previously shown to contain Caf1. It is not surprising that all three alleles of Caf1 in the current study are homozygous lethal, and that Caf1short cells have poor viability, considering that Caf1 has been found in the NURF and CAF-1 complexes, which have fundamental roles in nucleosome assembly and spacing. The apoptosis observed in eyes with Caf1short clones is also consistent with a role for Caf1 in the dREAM (Drosophila Rbf, E2F2, and Myb-interacting proteins) complex. Members of the E2f family of transcription factors can complex with Dp proteins and bind short recognition sites to activate transcription. When Rb binds the E2f-Dp complex, transcription is repressed. Like Caf1 homozygotes, homozygous rbf1 null flies die in early larval development. Fully rbf1-deficient embryos display increased apoptosis, a phenotype reminiscent of the increased active Caspase-3 staining seen anterior to the morphogenetic furrow in eye discs with Caf1short clones (Anderson, 2011).
The mammalian homologs of sens, Growth Factor Independence 1 (Gfi1) and Gfi1b are essential to the development of multiple cell types and have been implicated as oncogenes. Therefore, the possibility that Caf1 links Sens with the activity of PcG complexes through parallel, competing pathways has implications for both Drosophila development and the activity of Gfi1 family members in human development and disease, and warrants additional study beyond the scope of the present work. The results underscore the importance of Caf1 to diverse processes, including cell survival and tissue identity, and highlight the participation of Caf1 in multiple chromatin remodeling complexes. Further studies are needed to fully assess the importance of Caf1 in Drosophila development, as well as its developmental role in other chromatin remodeling complexes (Anderson, 2011).
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Chromatin assembly factor 1 subunit:
Biological Overview
| Evolutionary Homologs
| Regulation
| Developmental Biology
| Effects of RNAi
date revised: 10 June 2011
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