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How the body becomes asymmetric

Jan. 5, 2007
Special to World Science  

Re­search­ers say they’ve learn­ed a sur­pris­ing fact about cell di­vi­sion that might help ex­plain how we be­come asym­met­ric—with the heart on the left, and two dif­fer­ent brain halves, for in­stance.

The left-right dy­nein is one of 12 pro­teins form­ing the dy­nein mo­tor, a ti­ny ma­chine that per­forms trans­por­ta­tion tasks in a cell. The mo­tor is shown sche­mat­i­cal­ly above. Its two green, egg-shaped ends grab on­to a "microtubule," a type of struc­tur­al ca­ble with­in a cell. The op­po­site end of the mol­e­cule com­plex at­taches it­self to some "car­go." The green ends then "walk" along the cord to move the car­go. (Cour­te­sy ORNL.) 


It seems that when cells di­vide, they some­times dis­t­rib­ute their DNA dif­fer­ently among “daugh­ter” cells, said Amar J. S. Klar of the Na­tion­al Can­cer In­s­ti­tute at Fred­er­ick, Md. 

He and a col­league pre­sented a stu­dy on the sub­ject in in the Jan. 5 is­sue of the re­search jour­nal Sci­ence.

When cells re­p­ro­duce, they first rep­li­cate each of their chro­m­o­somes, which con­t­ain the genes. One copy of each chro­mo­some, called a chro­ma­tid, then goes to each daugh­ter cell. 

Sci­en­tists tra­di­tion­ally thought that for a giv­en chro­mo­some, which cell gets which chro­ma­tid is ran­dom. But Klar and Atha­na­sios Ar­mako­las, now at the Hip­po­kra­te­ion Hos­pi­tal of Ath­ens, found that in mice, this dis­tri­bu­tion is ran­dom in some cell types but not oth­ers.

When it’s not, the “bi­as” in dis­tri­bu­tion de­pends on the pres­ence of a pro­tein mol­e­cule called left-right dynein, the re­search­ers said. This is part of a small mo­lec­u­lar “mo­tor” be­lieved to drag chro­mo­somes to their des­ti­na­tions in daugh­ter cells.

The new find­ings thus sug­gest the pro­tein may also help de­cide which chro­ma­tid goes to which daugh­ter cell, Klar ar­gued.

How it might do this is un­known, but it’s “sus­pi­cious that a dynein mo­tor pro­tein—a fam­i­ly [of pro­teins] whose mem­bers are in­volved in chro­mo­some move­men­t—af­fect chro­ma­tid seg­re­ga­tion,” wrote Car­men Sapienza of Tem­ple Uni­ver­si­ty Med­i­cal School in Phil­a­del­phia, in a com­men­tary pub­lished with Klar’s pa­per in the jour­nal.

Pre­vi­ous stud­ies al­so found that left-right dynein af­fects the asym­me­try in bo­d­ily or­gans, said Klar. In 1959, Amer­i­can re­search­ers found that mice with mu­ta­tions in the gene for left-right dy­nein had a ran­domized struc­ture: half de­vel­oped in­sides that were mir­ror im­ages of the nor­mal.

It thus seems “very like­ly” that the asym­met­ric cell rep­li­ca­tion, due to this mo­lec­u­lar mo­tor, helps de­ter­mine the or­gan asym­me­try, Klar said. “The plot comes around in a cir­cle; it is too good to be a mere co­in­ci­dence,” he wrote in an e­mail.

In­di­vid­u­ally, though, each dynein-mutated mouse was still asym­met­ric, the 1959 study found. That is, or­gans in one in­di­vid­u­al would be slight­ly dif­fer­ent on the left and right. Thus, the dynein gene seems to de­ter­mine the dis­tri­bu­tion of asym­me­try—not the fact of asym­me­try it­self, Klar said. Sev­er­al oth­er genes are known to af­fect the lat­ter, he added, though these don’t re­late to mo­lec­u­lar mo­tors.


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Researchers say they’ve learned a surprising fact about cell division that might help explain how we become asymmetric—with the heart on the left, and two different brain halves, for instance. It seems that when cells divide, they sometimes distribute their DNA differently among “daughter” cells, said Amar J. S. Klar of the National Cancer Institute at Frederick, Md. He and a colleague presented a study on the subject in in the Jan. 5 issue of the research journal Science. When cells reproduce, they first replicate each of their chromosomes, which contain the genes. One copy of each chromosome, called a chromatid, then goes to each daughter cell. Scientists traditionally thought that for a given chromosome, which cell gets which chromatid is random. But Klar and Athanasios Armakolas, now at the Hippokrateion Hospital of Athens, found that in mice, this distribution is random in some cell types but not others. When it’s not, the “bias” in distribution depends on the presence of a protein molecule called left-right dynein, the researchers said. The protein is part of a small molecular “motor” believed to help drags chromosomes to their destinations in daughter cells. The new findings thus suggest the protein may help decide which chromatid goes to which daughter cell, Klar argued. How it might do this is unknown, but it’s “suspicious that a dynein motor protein—a family [of proteins] whose members are involved in chromosome movement—affects chromatid segregation,” wrote Carmen Sapienza of Temple University Medical School in Philadelphia, in a commentary published with Klar’s paper in the journal. Previous studies also found that left-right dynein affects the asymmetry in organs, said Klar. In 1959, American researchers found that mice with mutations in the gene that produces the proteins had a randomized structure: half developed insides that were mirror images of the normal. It thus seems “very likely” that the asymmetric cell replication, due to this molecular motor, ultimately leads to the organ asymmetry, Klar said. “The plot comes around in a circle; it is too good to be a mere coincidence,” he wrote in an email. Individually, though, each dynein-mutated mouse was still asymmetric, the 1959 study found. That is, organs in one individual would be slightly different on the left and right. Thus, the dynein gene seems to determine the distribution of asymmetry—not the fact of asymmetry itself, Klar said. Several other genes are known to affect the latter, he added, though these don’t relate to molecular motors.