Foreign Troubles Create Robust Buyers Market In US

first_img in Daily Dose, Data, News Freddie Mac Housing Market Mortgage Rates U.S. Housing 2016-07-12 Seth Welborn Recent international market blockbusters like China’s slowing economy and the U.K.’s decision to leave the European Union were significant enough for Freddie Mac to revise what it had expected to happen in the U.S. economy through the end of next year, but the GSE says the turbulence abroad has created a highly buyer-friendly mortgage market.Freddie Mac’s latest monthly outlook report, released Tuesday, stated that slowing growth in China and the June Brexit vote have played a major role in driving down mortgage rates. In the most recent Primary Mortgage Market Survey, Freddie Mac reported that the 30-year fixed-rate mortgage fell to 3.41 percent, just slightly above the all-time record low.“This,” the outlook report stated, “is likely to result in a boost in housing activity, particularly refinance, as homeowners take advantage of the current low rates.”Troubles overseas should also keep mortgage rates near historic lows, thereby allowing mortgage originations to surpass 2015’s level, the report stated.“The Federal Open Market Committee (FOMC) will likely keep the fed funds target rate increase on hold until at least the end of the year or even early next year,” Freddie Mac stated. “In its June meeting, the FOMC decided to keep the fed funds rate unchanged following a weaker than expected employment report for May as well as continued uncertainty in the global financial markets. Furthermore, following the results of the Brexit vote in late June, the Fed will likely continue to express caution before easing monetary accommodations.”According to Freddie Mac, the 30-year fixed-rate mortgage forecast has been revised down for both 2016 (by 30 basis points) and 2017 (by 50 basis points) to 3.6 percent and 4.0 percent, respectively.“Based on these low mortgage rates, expect the refinance share of originations to rise to 49 percent for 2016, 8 percentage points above last month’s forecast,” the report stated. “This translates to about $100 billion more in originations, bringing the total for 2016 to $1,825 billion.”The overall outlook is bolstered by June’s much-improved employment report.“Expect unemployment to average 4.9 percent in 2016 and 4.8 percent in 2017,” Freddie Mac reported.The house price appreciation forecast for 2016 remains at 5 percent, and at 4 percent for 2017. Foreign Troubles Create Robust Buyers’ Market In U.S.center_img July 12, 2016 627 Views Sharelast_img read more

Novel CRISPRderived base editors surgically alter DNA or RNA offering new ways

first_img (GRAPHIC) C. BICKEL/SCIENCE; (DATA) D. B. T. COX ET AL., SCIENCE 358, 6362, 2017 © SCIENCE; J. DOUDNA AND E. CHARPENTIER, SCIENCE 346, 6213, 2014 © SCIENCE; GAUDELLI ET AL., NATURE 551, 7677, 2017 Since the start of the CRISPR craze 5 years ago, scientists have raced to invent ever-more-versatile or efficient variations of this powerful tool, which vastly simplifies the editing of DNA. Two studies published in Science and Nature this week broaden CRISPR’s reach further still, honing a subtler approach to modifying genetic material that’s called base editing. One study extends a strategy for editing DNA, whereas the other breaks new ground by base editing its molecular cousin, RNA.Both open new avenues for genetic research and even curing diseases. “One shouldn’t view base editors as better than CRISPR—they’re just different,” says David Liu, a chemist at Harvard University who pioneered DNA base editing in a paper in Nature last year and co-authored the latest Nature paper. “It’s like, what’s better, a boat or a car?”CRISPR, adapted from a primitive bacterial immune system, does its handiwork by first cutting the double-stranded DNA at a target site in a genome. Base editing, in contrast, does not cut the double helix, but instead uses enzymes to precisely rearrange some of the atoms in one of the four bases that make up DNA or RNA, converting the base into a different one without altering the bases around it. That ability greatly increases the options for altering genetic material. “It’s a very worthwhile addition and it’s here to stay,” says CRISPR researcher Erik Sontheimer of the University of Massachusetts Medical School in Worcester. Novel CRISPR-derived ‘base editors’ surgically alter DNA or RNA, offering new ways to fix mutations Sign up for our daily newsletter Get more great content like this delivered right to you! 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DNA has four nucleotide bases—A, C, T, and G—and base editing changes one to another. In Liu’s 2016 study, his team fused gRNA with a “dead” Cas9 (dCas9) that cannot cut the whole double helix but still unzips it at the correct spot. To this complex the researchers tethered an enzyme, APOBEC1, which triggers a series of chemical reactions that ultimately change C to T. DNA’s base-pairing rules, which specify that a T on one DNA strand pairs with an A on the opposite strand, govern a subsequent change. The dCas9 was further modified to nick the unedited strand, which gooses the cell’s DNA repair mechanism into converting the G that originally paired with C into an A that pairs with the new T.That first DNA base editor could not address the most common point mutations associated with human diseases—accounting for about half—which have A•T where there should be G•C. The new editor from Liu’s group can now make this fix. The team again fused gRNA with a dCas9, but there is no known enzyme that can convert A to G in DNA. So the lab developed one from TadA, an enzyme in the bacterium Escherichia coli. The new enzyme converts A to a base called inosine, or I. Either a cellular repair mechanism or the process of the DNA copying itself then changes the I to a G. “The big deal here is engineering the TadA enzyme to do something fairly unnatural,” says George Church of Harvard, who studies CRISPR. “My hat is off to them.”Zhang’s team created its RNA base-editor system by fusing gRNA with a different dead nuclease, dCas13, and a natural enzyme that converts A to I in RNA. Unlike in DNA, that’s where the changes stop. The I-containing RNA simply performs as if it had a G in that spot.Because RNA carries the genetic message from DNA to the cell’s proteinmaking factories, or can directly perform acts such as gene regulation, it, too, is an appealing target for therapies. But an RNA only sticks around in a cell for a short time. That means RNA base editors likely would have to be repeatedly administered to work as a therapeutic, which Zhang and his co-authors suggest may make sense for transient conditions, such as localized inflammation.Although the short-lived nature of RNA makes base editing less attractive for many therapies, Sontheimer sees an upside, too. “In some ways, it’s safer to work on RNA,” he says. Researchers worry that genome editing could accidentally affect the wrong part of the genome—a change that would be permanent with a DNA base editor. “If there’s some degree of off targeting, you’re not permanently etching those mistakes into the underlying genome” with an RNA base editor, Sontheimer says.Church says base editing should be evaluated “case-by-case” for whether it offers advantages over CRISPR and other technologies that alter nucleic acids. “People make it sound like [changing bases] was not possible before. In fact it was hard or just inefficient,” he notes.Zhang and Liu stress that it could be several years before base-editing therapies enter clinical trials—and longer until it’s clear whether the strategy offers advantages over existing gene therapies. “It’s both scientifically short-sighted and long-term incorrect to conclude that base editing is going to be a better way to do human genetic therapy,” Liu says. What’s already clear, however, is that powerful alternatives to standard CRISPR are now in the game. Getting to the point of mutations Base editors borrow from CRISPR’s components—guide RNAs (gRNAs) and Cas9 or other nucleases—but don’t cut the double helix and instead chemically alter single bases with deaminase enzymes such as TadA and ADAR. Variations of the CRISPR DNA editor can change one DNA base into another. Email Click to view the privacy policy. Required fields are indicated by an asterisk (*) Many human diseases are caused by the mutation of a single base. CRISPR has difficulty correcting these so-called point mutations efficiently and cleanly, so base editing could provide a more effective approach. After Liu’s initial report, a group in China used DNA base editing to correct a disease-causing mutation in human embryos cloned from a patient with a genetic blood disorder.Conventional CRISPR uses a guide RNA (gRNA) coupled with an enzyme known as a nuclease, most commonly Cas9, that together attach to a specific stretch of DNA bases; the nuclease then snips the double helix. A cellular repair mechanism attempts to rejoin the cut DNA ends, but occasionally inserts or deletes bases, which turns the DNA code into gibberish and can knock out a targeted gene. “Gene editing based on nucleases is very good at inactivating genes,” says CRISPR researcher Feng Zhang of the Broad Institute in Cambridge, Massachusetts.Yet CRISPR, he notes, “is less efficient at making precise changes.” To fix a point mutation, a CRISPR-Cas9 system must also introduce a strand of “donor” DNA that has the correct base and then rely on a second cellular mechanism called homology-directed repair (HDR). But HDR works poorly unless cells are dividing, which means this strategy doesn’t function in, say, brain and muscle cells that no longer copy themselves. Even in dividing cells, the donor DNA rarely slots into the cut spot. By Jon CohenOct. 25, 2017 , 1:00 PMlast_img read more